Stroke Cancer Research Results
Stroke, Stroke: Click to Expand ⟱
| Source: |
| Type: |
| Stroke: A stroke, sometimes referred to as a brain attack arises if the blood flow is obstructed to a particular region of the brain or if the blood vessels in the brain rupture.
|
Scientific Papers found: Click to Expand⟱
*Stroke↓, Buckwheat is useful in prevention of strokes, many cardiovascular diseases
*cardioP↑,
*eff↑, BSAQ significantly exhibited astonishingly high contents of organic acids including oxalic acid, malic acid, citric acid and GABA.
*Dose↑, Contents of polyphenolics, rutin, quercetin and GABA all increased by 13%, 5%, 75%, and 6.7%, respectively (Table IV). Aquaculture in reality had improved much more production of these precious nutraceuticals
| - |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
*neuroP↑, EGb 761, a proprietary ginkgo leaf extract, has been shown to improve brain cell energy supply, to enhance neurogenesis and neuroplasticity, to decrease blood viscosity and improve brain perfusion.
*cognitive↑, Thereby it improves cognitive performance, neuropsychiatric symptoms and activities of daily living in patients with dementia or mild cognitive impairment.
*Stroke↓, It has further been shown to be beneficial for patients after ischaemic stroke.
*toxicity↓, The drug was shown to be safe and well tolerated and is a promising treatment option for patients developing dementia after cerebral infarction.
Dose↝, From the search results, we selected randomised placebo-controlled trials with a daily dose of 240 mg EGb 761
*Dose↝, A standardized formulation, EGb 761®, also sold as Tanakan® or Tebonin®, was created to normalize the constituents to assure reliable and consistent drug performance and the absence of ginkgolic acid, a known allergen naturally found in Ginkgo
*PAF↑, Ginkgolides have been clinically shown to act as platelet-activating factor (PAF) antagonists, inhibiting platelet aggregation and promoting increased blood flow.
*AntiAg↑,
*BloodF↑,
*Inflam↓, Additionally, BB(bilobalide) has shown anti-inflammatory properties and neuroprotection in preclinical models of stroke16 and AD
*neuroP↑,
*Stroke↓, Alternatively, promising results have been observed that support administration of EGb 761 soon after the onset of ischemia and during the recovery period.
*Dose↝, The standard clinical dose of EGb 761 is 120 mg (~1.7 mg/kg) once or twice daily; thus, a standard dose will contain ~3–4 mg ginkgolides A, B, and C, 3–4 mg BB, and 29 mg flavonoids.
*Sepsis↓, Patients treated with antimicrobials plus GB showed a significant drop in mortality as compared to patients treated with antimicrobials and placebo; this finding led to the development of other PAF antagonists for the treatment of sepsis
*memory↑, when administered daily, EGb 761 (240 mg daily) may improve some aspects of memory better than others
*Dose↑, Oral administration of EGb 761 at 25, 50 and 100 mg/kg/day and bilobalide at 3 and 6 mg/kg/day for 7 days before ischemia
*Stroke↓, These results suggest that oral administration of bilobalide and EGb 761 protect against ischemia-induced neuron death and reductions in mitochondrial gene expression.
AntiCan↑, Flavonoids possess a number of medicinal benefits, including anticancer, antioxidant, anti-inflammatory, and antiviral properties.
*antiOx↑,
*Inflam↓,
*AntiViral↑,
*neuroP↑, They also have neuroprotective and cardio-protective effects.
*cardioP↑,
*AChE↓, Apple peel extracts rich in flavonoids inhibits acetylcholinesterase (ACE) in vitro and is an effective antihypertensive agent [17,18,19,20]. It also prevents cardio-metabolic disorders [21] and displays better preservation of cognitive performance w
*cognitive↑,
Risk↓, Flavonoids present in apple are reported to reduce the risk of colorectal cancer. Studies have shown that consumption of one apple per day reduces the chance of cancer up to 50%
*Stroke↓, Stroke Prevention
*AntiDiabetic↑, Antidiabetic Effects
*AntiFungal↑, Antifungal Properties
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
PSA, |
NA |
|
|
|
BioAv↝, FMN has only one phenolic hydroxyl group, so it is poorly soluble in water and easily soluble in organic solvents such as methanol, ethyl acetate, and ether.
*memory↑, It had been found that FMN, isolated from Sophora secundiflora, could improve memory problems by restoring the level of oxidative stress in brain tissues and modulating acetylcholinesterase activity. I
*ROS↓, findings suggest that FMN can inhibit oxidative stress in the liver and restore mitochondrial function
*AChE↓,
*NF-kB↓, FMN, the expression levels of the above three decreased and NF-κB activation was inhibited, which may be related to the release of FMN blocking kelch-like ECH-associated protein-1 (Keap1) and activating the nuclear factor erythroid 2-related factor 2
*Keap1↝,
*NRF2↑,
*Inflam↓, FMN exerted anti-neuroinflammatory effects by targeting peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) and bidirectionally regulating NF-κB signaling pathway and Nrf2/Heme oxygenase-1 (HO-1) signaling pathway,
*PGC-1α↝,
*HO-1↓,
*p‑tau↓, thereby inhibiting tau protein hyperphosphorylation.
*cognitive↑, Significantly FMN improve cognitive dysfunction in mice caused by high-fat feeding
*BDNF↑, increased BDNF and 5-hydroxytryptamine (5-HT) levels, and mitigated the progression of depression in mice.
*5HT↑,
*Stroke↓, It could significantly reduce the level of inflammatory factors, increase the number of dendritic spines in neurons, and increase the expression of βIII-tubulin, growth-associated protein 43 (GAP-43), nerve growth factor (NGF) and BDNF.
*PARP1↓, FMN significantly reduced PARP1, PARG, apoptosis-inducing factor (AIF), cysteinyl aspartate-specific protease 3 (caspase-3) and p53 protein in rats with cerebral ischemia-reperfusion injury
*AIF↓,
*Casp3↓,
NP/CIPN↓, FMN had a favorable ameliorative effect on oxaliplatin-induced peripheral neuropathy and did not affect the chemotherapeutic function of oxaliplatin.
*neuroP↑, The neuroprotective mechanism of FMN is shown in Figure 2.
*NGF↑,
*TNF-α↓,
*IL1β↓,
*IL18↓,
*IL6↓,
*VCAM-1↓,
*pol-M2 MC↑,
*hepatoP↑, could reduce hepatotoxicity and improve liver function through inflammatory molecular pathways.
*AST↓, reduce serum AST, ALT, TNF-α and IL-1β levels. I
*ALAT↓,
*LC3II↑, the levels of LC3II, Beclin1, p62, cyclooxygenase-2 (COX2), COX4, MMP and adenosine triphosphate (ATP) were increased
*Beclin-1/ATG6↑,
*p62↑,
*COX2/PTGS2↑,
*MMP↑,
*ATP↑,
*GSH↑, activity of antioxidant proteins glutathione (GSH), catalase (CAT), GSH-PX in the FMN treatment group recovered, and the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) decreased.
*Catalase↑,
*GPx↑,
*MDA↓,
*antiPs↑, it was found that the interferon (IFN) signaling pathway was inhibited, which could effectively reduce the expression of related inflammatory chemokines, and significantly improve the erythema, scales and thickness of skin lesions in the psoriasis m
*AntiDiabetic↑, FMN effectively mitigated alloxan-induced pancreatic β-cell and DNA damage, lowered blood glucose levels, and increased insulin content.
*glucose↓,
*Insulin↑,
*GutMicro↑, FMN could act as a prebiotic to regulate intestinal microbial flora, thereby improving host metabolism and preventing obesity
*Obesity↓,
COX2/PTGS2↓, FMN effectively inhibited the proliferation of KYSE170 and KYSE150 cells by significantly reducing the mRNA and protein expression levels of COX-2 and cyclin D1, while inducing G1 phase arrest.
cycD1/CCND1↓,
TumCCA↑,
EGFR↓, FMN binds to both WT and mutant EGFR, reducing EGFR kinase activity and inhibiting downstream signaling.
GSK‐3β↑, This, in turn, activated GSK-3β and decreased the expression of myeloid leukemia sequence 1 (Mcl-1), without causing significant toxicity to the vital organs of mice.
Mcl-1↓,
*toxicity↓,
TumCP↓, FMN inhibited the proliferation and growth of cervical cancer cells by inhibiting the expression of HIF-1-α and VEGF.
Hif1a↓,
VEGF↓,
ERK↓, can achieve antiproliferative and invasive effects through effective inhibition of the oncogenic ERK1/2 pathway and the Lamin A/C signaling pathway,
LAMs↓,
Cyt‑c↑, FMN, as a candidate anticancer drug, could release cytochrome C (cyto C) directly through the mitochondrial pathway and activate the cascade reaction of caspase-9, caspase-3 and PARP, which ultimately lead to FaDu cell death
Casp9↑,
Casp3↑,
PARP↑,
TumCD↑,
mitA↑, FMN inhibited mitosis by inactivating the BACH1/p53 signaling pathway, promoted the release of cyto C
BACH1↓,
P53↓,
ROS↑, FMN delivered ROS to mitochondria to release cyto C and activated caspase-3 and caspase-9 cascade reactions to induce apoptosis in MCF7 cells
PD-1↓, FMN has the potential to serve as a PD-1/PD-L1 inhibitor for clinical use
NF-kB↓, FMN mainly interfered with PD-L1 activation by inhibiting the STING-NF-κB signaling pathway
*Bacteria↓, possess other pharmacological activities, such as antibacterial, antiviral, and antiallergic
*AntiViral↑,
*mt-ROS?, FMN effectively reduced the accumulation of ROS and mitochondrial damage in hair cells by activating the PI3K/AKT-Nrf2 signaling pathway, restored the balance of GSH/GSSG.
*PI3K↓,
*chemoP↑, FMN was a potential therapeutic agent for cisplatin-induced ototoxicity.
ChemoSen↑, Therefore, combination therapy had better control effects on multiple targets and a lower risk of drug resistance, which had great application prospects for treating cancer.
eff↑, combination of FMN (30 μM) and sulforaphane (20 μM) exhibited a significant synergistic effect
*toxicity↓, Therefore, it was proved that FMN was safe and non-toxic and could be used for pharmacological and therapeutic purposes.
*BioAv↑, water solubility problem of FMN, succinylated FMN using Bacillus amyloliquefaciens FJ18 to form the compound FMN-7-O-β-D (6″-O-succinyl)-D-glucoside (FMP), which compared to FMN, the water solubility was increased more than 106-fold.
*BioAv↑, To solve those problems, structural modification and nano-delivery systems can be used as a promising solution
*eff↑, FMN can be combined with other treatments, such as immunotherapy, to enhance the therapeutic effect and improve the prognosis of patients;
*toxicity↓, Promisingly, toxicity studies have shown that GA scarcely has obvious toxicity or side effects in a variety of animal experiments and clinical trials.
*Inflam↓, anti-inflammatory mechanisms of GA mainly involved MAPK and NF-κB signaling pathways.
*NF-kB↓,
AntiTum↑, GA also has several evident pharmacological effects including anti-tumor, anti-bacterial, anti-diabetes, anti-obesity, anti-microbial and anti-myocardial ischemia
Bacteria↓,
*AntiDiabetic↑,
*Obesity↓,
*AntiBio↑,
*Stroke↓,
*NO↓, GA could inhibit the secretion of pro-inflammatory mediators nitrite, NO, PGE2 and IL-6 in a dose-dependent manner
*PGE2↓,
*IL6↓,
*MAPK↓, GA inhibits the activities of NF-κB and MAPK, subsequently inhibiting the release of inflammatory factors (TNF-α, IL-1β/6), chemokines (CCL-2, ICAM-1, TIMP-1)
*TNF-α↓,
*IL1β↓,
*MCP1/CCL2↓,
*ICAM-1↓,
*TIMP1↓,
*NRF2↑, activate several signalling mechanisms in cells, including the Nrf2 pathway, which is the master controller of the antioxidant defence that detoxifies reactive oxygen species (ROS)
*ROS↓,
*Stroke↓, GBE or its component antioxidants could be applied for the treatment and/or prevention of DN, ischemic stroke
*Stroke↓, Ginkgo biloba use was also associated with an improvement in activities of daily living and functional outcome
*eff↑, Subgroup analysis suggest that the impact was larger when using an injectable formulation of Ginkgo biloba compared to the oral formulation.
*toxicity↓, no apparent impact of Ginkgo biloba use on all-cause mortality (Risk ratio (RR): 1.21; 0.29-5.09, p=0.80) or cerebrovascular bleeding
*other?, more studies are needed before it can be recommended for routine use in improving neurological and cognitive function in patients with acute ischemic stroke
*neuroP↑, Ginkgolide B (GB), a key component of Ginkgo biloba extract, has shown potential neuroprotective effects, but its pro-angiogenic mechanisms remain unclear.
*VEGF↑, GB treatment significantly increased VEGF and Ang expression (p < 0.01), likely via AKT1 upregulation
*AKT1↑,
*angioG↑, GB promotes angiogenesis and exerts neuroprotective effects by activating the AKT1/VEGF/Ang signaling pathway,
*Stroke↓, suggesting its potential therapeutic value for ischemic stroke-related injuries.
*Dose↝, 6-Shogaol is formed from 6-gingerol by dehydration and represents one of the main bioactive principles in dried ginger rhizomes.
*Inflam↓, In vitro and in vivo, 6-shogaol reduced inflammatory mediator systems such as COX-2 or iNOS, affected NFκB and MAPK signaling, and increased levels of cytoprotective HO-1.
*COX2/PTGS2↓,
*iNOS↓,
*NF-kB↓,
*MAPK?,
*HO-1↑,
*PGE2↓, Rat/saline administration 50 and 500 mg/kg extract oral or i.p. Reduced PGE2 serum levels
*TNF-α↓, 25, 50, 100 and 200 mg/kg extract oral Reduced carrageenan-induced paw volume, levels of PGE2, TNF, IL-6, IL-1β, IFNγ, MCP-1, MIP-2, RANTES, and MPO activity and NO levels
*IL6↓,
*IL1β↓,
*IFN-γ↓,
*MCP1/CCL2↓,
*MIP2↓,
*RANTES↓,
*MPO↓,
*NO↓,
*Stroke↓, Therefore, the authors of this study suggest a potential benefit of 6-shogaol for the prevention of stroke [51].
*BrainVol↑, The daily oral administration of 6-shogaol (5 and 20 mg/kg) resulted in protection against transient focal cerebral ischemia, as indicated by a significant reduction of brain infarct volume and production of malondialdehyde (MDA) and of ROS after MCA
*MDA↓,
*ROS↓,
*GSH↑, 6-shoagol treatment resulted in an increased amount of glutathione (GSH) in H2O2-induced HepG2 cells
*NRF2↑, As H2O2-triggered Nrf2 degradation was recovered by 6-shogaol,
*antiOx↑, 6-Shogaol exhibits a stronger antioxidative activity than its homologues
NLRP3↓, 6-shogaol (20 µM) effectively inhibited total protein levels of NLRP3 and pro-IL-1β after a combined LPS and ATP-activated protein up-regulation
HDAC1↓, The LPS-caused induction of HDAC1 protein levels was reduced by 6-shogaol
*Inflam↓, anti-inflammatory, antioxidant, antifibrotic, anticancer, neuroprotective, cardioprotective, metabolic regulatory and antibacterial activities.
*antiOx↓, GK markedly attenuates oxidative stress in diverse experimental models.
AntiCan↑,
*neuroP↑,
*cardioP↑,
*Bacteria↓,
*ROS↓, GK significantly reduces intracellular ROS levels and lipid peroxidation products in various cell lines under metabolic or inflammatory stress
*lipid-P↓,
*NRF2↓, Both in vitro and in vivo studies consistently show that GK upregulates Nrf2 expression and nuclear translocation while downregulating Keap1,
*Keap1↓,
*NF-kB↓, numerous in vitro and in vivo studies have demonstrated that GK suppresses the NF-κB pathway
*MAPK↓, animal models show that GK attenuates MAPK pathway activation
MMP2↓, In vitro and in vivo evidence indicates that GK downregulates matrix metalloproteinases, including MMP-2 and MMP-9
M2 MC↓,
JAK2↓, In multiple cancer models, GK suppresses the JAK2/STAT3 signaling axis, leading to reduced expression of proliferation- and survival-related genes
STAT3↓,
TumCP↓,
Casp↑, GK induces mitochondrial-dependent apoptosis characterized by caspase activation and modulation of Bcl-2 family proteins
ChemoSen↑, GK can synergize with conventional chemotherapeutic agents.
*BMD↑, figure 4
*Aβ↓, In Alzheimer’s disease, GK directly targets Aβ pathology by inhibiting β-secretase and modulating fibril formation, while in vivo it reduces Aβ burden and neuroinflammation, partly via NF-κB pathway suppression
*Stroke↓, In ischemic stroke and cerebral ischemia–reperfusion injury, GK consistently improves neurological outcomes by modulating interconnected pathways.
*BioAv↓, GK exhibits relatively low oral bioavailability due to its biflavonoid structure and high lipophilicity, which result in poor aqueous solubility and limited intestinal absorption
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*AntiCan↑, Ginkgetin (GK), a natural non-toxic biflavone, has been shown to exhibit anti-cancer, anti-inflammatory, anti-microbial, anti-adipogenic, and neuroprotective activities.
*Inflam↓,
*AntiBio↑,
*neuroP↑,
*TumCCA↑, GK combats cancer progression by arresting cell cycle, inducing apoptosis, stimulating autophagy, and targeting many deregulated signaling pathways such as JAK/STAT and MAPKs.
Apoptosis↑,
TumAuto↑,
iNOS↓, GKhalts inflammation mediators like interleukins, iNOS, COX-2, PGE2, NF-κB, and acts as an inhibitor of PLA2
COX2/PTGS2↓,
PGE2↓,
NF-kB↓,
PLA2↓,
*neuroP↑, GK shows strong neuroprotection against oxidative stress-promoted cell death, inhibits cerebral micro-hemorrhage, decreases neurologic deficits, and halts apoptosis of neurons
*Stroke↓, in cerebral ischemia rat model, GK significantly improved I/R-stimulated neurological deficit scores
*AntiFungal↓, GK also acts as anti-fungal, anti-viral, anti-bacterial, leishmanicidal and anti-plasmodial agent.
*Bacteria↓,
Bcl-xL↓, steosarcoma cells, GK significantly suppressed the levels of B-cell lymphoma-extra-large (Bcl-xL) and B-cell lymphoma 2 (Bcl-2) proteins while significantly elevated levels of caspase-9 and -3 along with cleaved poly ADP ribose polymerase (PARP)
Bcl-2↓,
Casp9↑,
Casp3↑,
cl‑PARP↑,
IL6↓, GK selectively repressed the proliferation of prostate tumor via repressing interleukin 6 (IL-6)-induced as well as constitutive activation of STAT3
STAT3↓,
JAK1↓, GK abrogated the constitutive activation of both Src and JAK1 kinases which in turn halted STAT3 activation in FaDu and A549 cells.
survivin↓, suppressed its target genes including survivin, cyclooxygenase-2 (COX-2), inhibitor of apoptosis protein-1 (IAP-1), Bcl-xL, Bcl-2, matrix metalloproteinase 2 and 9 (MMP-2 and -9)
COX2/PTGS2↓,
IAP1↓,
MMP2↓,
MMP9↓,
PTEN↑, GK prompted the mRNA and protein expression of phosphatase and tensin homolog (PTEN) and SHP-1 which also paly role in STAT3 activation
SHP1↑,
eff↑, When GK is applied in combination with resveratrol, they synergistically act to suppress endothelial cell proliferation, migration, and reactive oxygen species (ROS) production as compared to mono drug
TumVol↓, GK decreased the weight and volume of tumor by 67.4% and 65.6%, respectively in the DU-145 xenografted mice model as compared to control and no toxic effect towards normal cells had been observed
TumW↓,
*toxicity↓,
*ROS↓, mediated neuronal cell damage in vitro by reducing intracellular ROS and maintaining MMP
| - |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Park, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
*neuroP↑, There is evidence of protection against neuronal damage caused by ischemic strokes, neurotumors, Alzheimer’s disease (AD), and Parkinson’s disease (PD).
*ROS↓, Possible mechanisms include inhibition of reactive oxygen species, inhibition of β-secretase, inhibition of Aβ fibril formation, amelioration of inflammation, and antimicrobial activity.
*Aβ↓,
*Inflam↓,
*Dose↝, Thus, ginkgetin consists of apigenin and apigenin 7,4′-dimethyl ether.
*cardioP↑, figure2
TumCCA↑, ginkgetin combats cancer progression by various mechanisms such as arresting the cell cycle, inducing apoptosis, stimulating autophagy, and targeting many deregulated signaling pathways such as JAK / STAT and MAPKs
Apoptosis↑,
TumAuto↑,
STAT↓,
*Stroke↓, Protection against Neuronal Injury Caused by Ischemic Stroke
*Stroke↓, Our results showed that administration of ginkgetin remarkably reduced brain infarction volumes and neurologic deficits;
*Apoptosis↓, reducing apoptotic cell numbers, downregulating the levels of cleaved caspase-3 and Bax, and upregulating the level of Bcl-2 in rats subjected to IR injury in a dose-dependent manner.
*Casp3↓,
*BAX↓,
*Bcl-2↑,
*p‑Akt↑, high-dose ginkgetin treatment (100 mg/kg) significantly increased the phosphorylations of Akt and mTOR.
*p‑mTOR↑,
*BioAv↑, GSPE is highly bioavailable and provides significantly greater protection against free radicals and free radical-induced lipid peroxidation and DNA damage than vitamins C, E and beta-carotene.
*ROS↓,
AntiCan↑, GSPE was also shown to demonstrate cytotoxicity towards human breast, lung and gastric adenocarcinoma cells, while enhancing the growth and viability of normal human gastric mucosal cells.
selectivity↑,
RenoP↑, GSPE also demonstrated excellent protection against acetaminophen overdose-induced liver and kidney damage by regulating bcl-X(L) gene, DNA damage and presumably by reducing oxidative stress.
*hepatoP↑,
*DNAdam↓,
*Stroke↓, GSPE demonstrated excellent protection against myocardial ischemia-reperfusion injury and myocardial infarction in rats.
*Bcl-2↑, GSPE was also shown to upregulate bcl(2) gene and downregulate the oncogene c-myc.
cMyc↓,
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
IBD, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
- |
Review, |
Sepsis, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.
*Dose?, received inhalation of 67% high concentration of hydrogen gas for 60 min once a day for 7 consecutive days after OVA or PBS challenge respectively
*IL4↓, Increased level of IL-4, IL-13, TNF-α and CXCL15 in the BALF and IL-4 in the serum were decreased significantly after inhalation.
*IL13↓,
*TNF-α↓,
*CXCL15↓,
*SOD↑, Hydrogen gas inhalation markedly upregulated the activity of decreased superoxide dismutase
*MDA↓, and significantly attenuated the increased level of malondialdehyde and myeloperoxidase
*MPO↓,
*ROS↓, Hydrogen gas inhalation improves lung function and protects established airway inflammation in the allergic asthmatic mice model which may be associated with the inhibition of oxidative stress process.
*antiOx↑, therapeutic effects of molecular hydrogen on various diseases have been investigated regarding its antioxidation capability [4] and its anti-inflammation [5] and anti-apoptosis
*Inflam↓,
*Apoptosis↓,
*toxicity↓, it is sufficiently mild that it does not disturb metabolic oxidation-reduction reactions or ROS-mediated cell signalling. Thus, it may be a safe and effective antioxidant for pulmonary diseases
*Stroke↓, , accumulating evidence has demonstrated various types of diseases involving oxidative stress, including ischaemic heart disease [7], stroke [8], acute lung injury [9] and inflammatory bowel disease
*Airway↓, Hydrogen gas inhalation decreased lung resistance in the asthmatic mice model
*Neut↓, There was a significant increase in the number of total cells, neutrophils , eosinophils , lymphocytes . Hydrogen gas inhalation resulted in significant reduction in the number of total cells
*Eos↓,
*BALF-Lym↓,
*BALF-Infl↓, Hydrogen gas inhalation attenuated the elevated levels of inflammatory cytokines present in BALF from the asthmatic mouse model
*AirwayM↓, In our study, we found the hydrogen gas inhalation significantly alleviated the pathologic inflammation degree and mucus content in the lung tissue.
*IL8↓, decreased IL-8 level only in asthma group
*IL4↓, IL-4 and IL-6 levels in EBC were significantly lower after inhalation in the COPD (0.80–0.64 pg/mL, P = 0.025) and asthma (0.06–0.05 pg/mL, P = 0.007) group, respectively.
*IL6↓,
*Inflam↓, A single inhalation of hydrogen for 45 min attenuated inflammatory status in airways in patients with asthma and COPD
*Sepsis↓, has been demonstrated that hydrogen could provide protection against various diseases, including sepsis, stroke and ischemia-reperfusion injury
*Stroke↓,
*antiOx↑, Hydrogen, which exhibits anti-oxidative and anti-inflammation effects, was proved to be relatively safe for inhalation in diving.9
*toxicity↓,
*AntiCan↑, anticancer, anti-inflammatory, antibacterial, antiviral, antidepressant, and organ protective effects.
*Bacteria↓,
*AntiViral↑,
*antiD↓,
*RenoP↑, Kidney protection
*hepatoP↑, Liver protection
*eff↑, treating multiple diseases, such as sepsis, arthritis, colitis, diabetic nephropathy, myocardial ischemia-reperfusion, pulmonary fibrosis, and cancers.
*Sepsis↓,
*AntiArt↑,
*Stroke↓,
TumCMig↓, hyperoside has been shown to inhibit the migration and invasion properties of A549 cells by suppressing the expression of metastasis-associated gene 1 (MTA1), matrix metalloproteinase-2 inhibitor (TIMP-2), matrix metalloproteinase (MMP)-2
TumCI↓,
MTA1↓,
TIMP2↓,
MMP2↓,
MMP↓, disrupted the penetration of the mitochondrial membrane, and triggered mitochondrial cytochrome C and apoptosis inducers into the cytoplasm
Cyt‑c↑,
Akt↓, inhibited the Akt/mTOR/p70S6K signaling pathway in NSCLC cells to promote autophagy and exerted anticancer activity
mTOR↓,
P70S6K↓,
TumAuto↑,
PD-L1↓, thereby inhibiting PD-L1 expression at the transcriptional leve
TNF-α↓, subsequently, inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1b, IL-6 and IL-8, were significantly down-regulated
IL1β↓,
IL6↓,
IL8↓,
Bcl-2↓, Hyperoside was reported to inhibit the over-expression of B-cell lymphoma factor 2 (Bcl)-2 and Bcl-x in lung cancer cells, and up-regulate the preapoptotic factors such as Bax, Bad, and Bak.
Bcl-xL↓,
BAX↑,
BAD↑,
Bak↑,
VEGF↓, decreasing the HeLa cell's vascular endothelial growth factor (VEGF) expression levels in HeLa cells.
Casp3↑, hyperoside promoted apoptosis via enhancing caspase-3 and caspase-8 protein expression, and on the other hand, by promoting tumor suppressor gene P35 expression
Casp8↑,
P53↑,
GSH↓, Hyperoside could also reduce glutathione levels in HeLa cells, superoxide dismutase (SOD), and Catalase (CAT) viability.
SOD↓,
Catalase↓,
TAC↓, reduced the antioxidant capacity and thus to inhibit cancer cell growth
XIAP↓, MCF-7 and 4 T1 cells Decreased the levels of Bcl-2 and XIAP; increased the levels of Bax and cleaved cysteine protease-3; decreased the production of ROS and inhibited NFκB signal pathway
ROS↓,
NF-kB↓,
TLR4↓, MDA-MB-231 cells Inhibited TLR4-NF-κB signaling pathways; decreased the expression of Bcl-2; enhanced the expression of pro-apoptotic Bax and the level of pro-inflammatory cytokine IL-6
P-gp/ABCB1↓, S180 cancer cell Reduced the expression of P-gp, LRP and Bcl-2 and increased the expression of Fas; inhibited bad phosphorylation and increased p27 level
LRP1↓,
Fas↑,
p27/CDKN1B↑,
*cardioP↑, Cardiovascular protection In vivo pulmonary embolism and arterial thrombosis model Prolonged the activated prothrombin time and suppressed thrombin and FXa activities; inhibit the production of PAI-1 induced by TNF-α
*AntiThr↑,
*PAI-1/SERPINE1↓,
*BUN↓, Reduced the contents of serum angiotensin converting enzyme ArgII, ALD, U-mAlb, BUN, SCR, ALT, and AST
*ALAT↓,
*AST↓,
*neuroP?, Neuroprotection
| - |
Review, |
Nor, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*RenoP↓, Thirdly, long-term use of hyperoside is toxic to the kidneys, but the damage is reversible
Casp3↑, Up-regulates caspase-3, caspase-8, Bax, p53 and MDA contents; decreases GSH, SOD and CAT activities; decreases VEGF and Bcl-2 levels; and inhibits cell growth. HeLa 100 μmol/L
Casp8↑,
MDA↑,
GSH↓,
SOD↓,
Catalase↓,
VEGF↓,
Bcl-2↓,
TumCG↓,
p‑Akt↓, Down-regulates BMP-7 expression, AKT phosphorylation and PI3K expression; induces cell cycle arrest; and inhibits cell proliferation. Human HepG2 5, 10, 20, 40 and 80 μM
PI3K↓,
TumCCA↑,
TumCP↓,
BMP7/OP1↓,
*ZO-1↑, up-regulates ZO-1 and claudin5 protein expression; maintains the integrity of the blood–brain barrier; and may protect neural function in CIR-injured mice. CIR injury induced by MCAO in mice 50 mg/kg
*BBB↝,
*p‑Akt↑, increases the phosphorylation of AKT and GSK-3β; alleviates early brain injury after subarachnoid haemorrhage; and promotes nerve function recovery in rats.
*GSK‐3β↑,
*SOD↑, increases SOD and CAT activities and GSH content; increases SIRT1 gene expression; down-regulates NF-κB mRNA
*Catalase↑,
*GSH↑,
*SIRT1↑,
*NF-kB↓,
*IL1β↓, Down-regulates IL-1β, IL-6, IL-8, TNF-α, ROS, MDA, Bax and caspase-3 levels; increases CAT, SOD and GSH activities; up-regulates Bcl-2, BDNF, TrkB, SIRT1 and NGF expression; reduces LPS-induced inflammation, oxidative stress and apoptosis; and protec
*IL6↓,
*IL8↓,
*TNF-α↓,
*ROS↓,
*MDA↓,
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BDNF↑,
*TrkB↑,
*NGF↑,
*Apoptosis↓,
*cardioP↑, Cardioprotective Activity of Hyperoside.
*AST↓, Decreases the levels of AST, CK, CK-MB and c-TnT in rats; the rate of cardiomyocyte apoptosis;
*hepatoP↑, Hepatoprotective Activity of Hyperoside.
*AST↓, Decreases liver index, AST, ALT, MDA and Bach1 complex levels and alleviates the pathological damage of acute liver injury mice.
*ALAT↓,
*MDA↓,
*BACH1↓,
*neuroP↑, Brain-Protective Activity of Hyperoside.
*Stroke↓, Down-regulates TNF-α, IL-1β, IL-6, ICAM-1, VCAM-1, TLR4, COX-2, NF-κB, caspase-3, caspase-9, Bax and Bcl-2 expression and prevents CIR injury. Middle cerebral artery occlusion/reperfusion rat model
*ICAM-1↓,
*VCAM-1↓,
*TLR4↓,
*COX2/PTGS2↓,
*RenoP↑, Renal-Protective Activity of Hyperoside.
*NLRP3↓, Suppresses NLRP3, caspase-1 and ASC expression and prevents acute kidney injury induced by lipopolysaccharide. Mouse acute kidney injury model
*Casp1↓,
*ASC↓,
*BioAv↓, low oral bioavailability
*BioAv↑, hyperoside is compatible with other traditional Chinese medicines and they can improve its bioavailability and oral absorption.
*toxicity↓, Firstly, an acute toxicity test of hyperoside showed that its LD50 > 5000 mg/kg
*ROS↓, ISL significantly attenuated H/R-triggered production of reactive oxygen species in NMCM, reduced the expression of malondialdehyde and the activity of lactate dehydrogenase, enhanced superoxide dismutase and catalase activity,
*MDA↓,
*LDH↑,
*SOD↑,
*Catalase↑,
*NRF2↑, and increased the expression of nuclear factor E2-related factor 2 (Nrf2) and its downstream heme oxygenase 1 (HO-1), thereby mitigating oxidative stress damage.
*i-Iron↓, ISL reduced intracellular free iron accumulation, up-regulated glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression, and inhibited lipid peroxidation accumulation, thereby alleviating ferroptosis.
*GPx4↑,
*xCT/SLC7A11↑,
*lipid-P↓,
*Ferroptosis↓,
*HO-1↑, ISL treatment increased the levels of HO-1, GPX4, and SLC7A11, inhibited the expression of ACSL4
*ACSL4↓,
*mtDam↓, alleviated mitochondrial damage, and ferroptosis, ultimately reducing myocardial infarction area and injury induced by I/R.
*Stroke↓,
*antiOx↑, Isoliquiritigenin (ISL) (PubChem CID:638278) exhibits a diverse range of pharmacological activities, including antioxidant, anticancer, and anti-tumor properties.
*AntiCan↑,
*AntiTum↑,
*AntiDiabetic↑, possess therapeutic effects on various diseases, such as diabetes, cardiovascular diseases, kidney diseases, and cancer, through the activation of the Nrf2 pathway.
*cardioP↑,
*RenoP↑,
*NRF2↑,
*NQO1↝, modulating the expression of antioxidative enzymes such as nicotinamide adenine dinucleotide phosphate quinone oxidoreductase-1(NQO1), heme oxygenase-1 (HO-1), superoxide dismutase (SOD) et al.
*HO-1↑,
*SOD↑,
*toxicity↓, ISL has been widely recognized as a safe phytochemical without any significant toxic, genotoxic, teratogenic properties in treating diseases
*BioAv↓, The research has determined that the bioavailability of ISL in rats following oral administration ranged from 22.70% to 33.62%, indicating a low level of oral bioavailability.
*Half-Life↓, distribution half-life of ISL was found to be 0.3 h, while the elimination half-life for ISL doses of 10, 20, and 50 mg/kg were determined to be 4.9, 4.6, and 4.8 h
*BBB↑, ISL can traverse the blood-brain barriers and exhibit neuroprotective effects in male MCAO-induced focal cerebral ischemic injury
*neuroP↑,
*Stroke↓,
*GSK‐3β↓, he protective effects of ISL have been shown to be exerted through inhibiting GSK-3β activity through increasing the expression levels of phosphorylated (p)-GSK-3β,
*p‑GSK‐3β↑,
*hepatoP↑, ISL has demonstrated its potential as a hepatoprotectant and as a means to mitigate the detrimental impacts of other substances on liver function
*Inflam↓, ISL has demonstrated efficacy in preventing inflammatory bowel disease
*ROS↓, The findings revealed that treatment with ISL effectively reduced the ROS production and attenuated cellular toxicity in RAW.264.7
*MPO↓, ISL has been found to inhibit the production of ROS, myeloperoxidase (MPO), and malondialdehyde (MDA).
*MDA↓,
| - |
in-vitro, |
Stroke, |
SH-SY5Y |
|
|
|
*Apoptosis↓, ISO treatment reduced the level of apoptosis in OGD/R-treated SH-SY5Y cells ISO rescued OGD/R-treated cells
*NRF2↑, Mechanistically, the expression of Nrf2 and ALDOC was upregulated upon ISO treatment
*ALDOC↑,
*neuroP↑, Our data revealed that ISO exhibited neuroprotective activity in OGD/R model through Nrf2-ALDOC-autopagy axis and highlighted the potential application of ISO in stroke treatment.
*Stroke↓,
| - |
Review, |
Nor, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*antiOx↑, anti-oxidant, anti-cancer, anti-inflammatory, anti-hyperalgesic, and neuroprotective effects.
*AntiCan↑,
*Inflam↓,
*neuroP↑,
*AChE↓, Anti-Alzheimer's disease Vitexin/isovitexin In vitro ChE enzyme assay Vitexin: IC 50 = 12.16 ± 3.58 (AChE) IC 50 = 6.73 ± 0.08 (BChE) IC 50 = 51.07 ± 3.31(BACE1) Isovitexin: IC 50 = 6.24 ± 1.15 (AChE) IC 50 = 6.48 ± 0.43 (BChE) IC 50 ≥ 100 (BA
*BChE↓,
*BACE/β-secretase↓,
*Stroke↓, Data showed that vitexin exhibits protective effect against cardiac ischemia/reperfusion (I/R) injury through inhibiting the I/R-induced decrease in coronary flow
*AntiAg↓, Vitexin-containing lime leaf significantly inhibited platelet aggregation in a concentration-dependent manner
*AntiDiabetic↑, Administered orally, vitexin and isovitexin significantly reduced postprandial blood glucose both in sucrose loaded normoglycemic mice and sucrose induced diabetic rat
*AGEs↓, vitexin and isovitexin, as AGE inhibitors,
*IL1β↓, inhibition in the pro-inflammatory cytokines such as IL-1β, IL6, IL-8, TNF-α,
*IL6↓,
*IL8↓,
*TNF-α↓,
*Obesity↓, Protective effects against obesity
*BioAv↝, Unusually, vitexin and isovitexin are poorly absorbed in the gastrointestinal tract [61]. They directly reached the colon where they were hydrolysed by the gut microflora through deglycosylation and ringopening of the heterocyclic C ring
*BioAv↓, oral bioavailability of vitexin was much low (approximately 5%
chemoPv↑, Both in vitro and in vivo studies suggest that vitexin and isovitexin are chemopreventive compounds with activity against various cancers through proapoptotic processes and/or autophagy.
Dose↝, Vitexin and isovitexin are the main constituents of the fruits of Cucurbitaceae, mung beans (Vigna radiata), pigeon pea leaves (Cajanus cajan Millsp.), bamboo leave
ACE/ACE1↓, Experimental studies showed that flavone C-glycosides act as angiotensin-converting enzyme (ACE) inhibitors and have vasodilatory, -blocking, and/ or Ca 2+ channel-blocking activities.
Ca+2↓,
*iNOS↓, C-glycosides reduced lipopolysaccharide-induced proinflammatory cytokine secretion, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 expression
*COX2/PTGS2↓,
*ROS↓, and reactive oxygen species (ROS) generation
*Stroke↓, provide protective effects against myocardial ischemia–reperfusion injury.
Apoptosis↑, Vitexin-triggered apoptosis was generally accompanied by a decrease in mitochondrial membrane potential and Bcl-2 protein levels, as well as an increase in caspase-3 and caspase-9 protein expression.
MMP↓,
Bcl-2↓,
Casp3↑,
Casp9↑,
TumAuto↑, In heat stress–related research, vitexin promoted autophagy through the upregulation of Hsp90 expression and subsequent activation of endoplasmic reticulum stress.
HSP90↑,
ER Stress↑,
Hif1a↓, vitexin and isovitexin was found in PC12 and CORL-23 cells by inhibiting hypoxia-inducible factor 1 (HIF-1a)
TumMeta↓, resulting in the reduction of the metastatic prospective of PC12 and CORL-23 cells and angiogenesis.
angioG↓, They are prominent antiangiogenic potential agents
Tf↓, Isovitexin and vitexin were found to bind to transferrin (TF), 38 one type of iron-binding glycoprotein that is highly expressed in fast-growing cells, including cancer cells
MAPK↓, Molecular targets for flavone C-glycosides comprise the mitogenactivated protein kinase (MAPK), protein kinase C (PKC), PI3K-Akt, and -catenin pathways
PI3K↓,
Akt↓,
β-catenin/ZEB1↓,
TumCCA↑, Vitexin inhibited growth and induced cell cycle arrest at G1 /G0 by regulating the Akt/FOXO3a pathway
FOXO3↓,
mTOR↓, Vitexin inhibits choriocarcinoma via inducing cell apoptosis and suppressing the mTOR pathway
| - |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
- |
Review, |
Park, |
NA |
|
|
|
*neuroP↑, it was speculated that vitexin, isovitexin, sinapic acid, and ferulic acid might be the major bioactive compounds for mung bean-mediated neuroprotection.
*Aβ↓, inhibition of β-amyloidogenesis, tau hyperphosphorylation, oxidative stress, and neuroinflammation, and promotion of autophagy and acetylcholinesterase enzyme activity.
*p‑tau↓,
*ROS↓,
*Inflam↓,
*AChE↓, vitexin significantly inhibited the activity of AChE in vitro, with an IC 50 of 12.16 μM.
*BBB↑, Notably, considerable levels of vitexin and isovitexin were detected in the brain, indicating their ability to cross the blood brain barrier (BBB)
*memory↑, Another study showed that mung bean sprout possessed anti-Alzheimer potential as evidenced by the improved short-term and long-term memory as well as inhibited AChE activity and oxidative stress after administering mung bean sprout for 15 days in mic
*hepatoP↑, That is, except for neuroprotection, mung bean can also provide several other health benefits, such as hepatoprotection, immunomodulation, antihyperglycemia, antihyperlipidemia, antihypertension, and anticancer
*Imm↑,
*hyperG↓,
*AntiCan↑,
*eff↑, neuroprotective potential of seed coat extract might be much stronger than that of cotyledon extract.
*Stroke↓, Vitexin showed great activities in improving CNS-related diseases, including AD, ischemic stroke, and Parkinson’s disease.
*BACE/β-secretase↓, vitexin suppressed the production of Aβ through downregulating the activity of β-secretase (BACE-1) with an IC 50 of 51.07 μM in vitro
*PI3K↓, Isovitexin was found to inhibit the activation of the PI3K/AKT/mTOR pathway, which might explain the molecular targets for isovitexin.
*Akt↓,
*mTOR↓,
*Dose↓, At the fifth day of sprouting, contents of vitexin and isovitexin decreased by 3.7 and 9.3 times, respectively
*other↓, melatonin production declines significantly with age, which may contribute to the development of age-related neurological disorders due to reduced levels.
*neuroP↑, neuroprotective effects of melatonin in cerebral ischemia-reperfusion injury.
*Stroke↓, The neuroprotective benefits of melatonin in experimental stroke models are well documented. Several studies have demonstrated a reduction in infarct size and cerebral edema volume, along with improved neurological function
*Dose↝, healthy individuals was found to be 69. 70 pg/ml in the systemic circulation. However, patients with stroke had lower melatonin levels, with an average of 48. 1 ± 35. 9 pg/ml.
*Risk↓, The reduction in melatonin levels was found to be associated with the occurrence of stroke. 1 pg/mL decrease in melatonin levels and a greater than 2% increase in stroke risk
*cognitive↑, studies suggest that melatonin improves cognition and regulates neuroplasticity to mitigate neurodegenerative processes
*neuroP↑, This study highlights the neuroprotective role of selected polyphenols through the PI3K/Akt pathway.
*other↝, Docking results also exhibited the strong to moderate affinity of the selected ligands (Apigenin, Ellagic acid, Ferulic acid, Kaempferol, Genistein, Luteolin, Naringenin, and Quercetin) towards the selected disease target.
*Stroke↓,
| - |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
- |
Review, |
Park, |
NA |
|
|
|
*Stroke↓, quercetin improved AD, ischemic stroke, and Parkinson’s disease, as well as aging, neuroinflammation, and daily intakes of advanced glycation end products (AGEs) or alumimum-induced cognitive impairments.62
*Inflam↓,
*AGEs↓,
*cognitive↑, quercetin (100 mg/kg, intragastrically, i.g.) to 6 month old 3xTg-AD mice for one year significantly prevented cognitive impairments, β-amyloidosis, and tauopathy.
*memory↑, clinical trial indicated that the memory recall improved in the early stage AD patients who consume quercetin-enriched onion powder
*Dose↝, (containing 80 mg quercetin aglycone) daily for 4 weeks compare to those who take white onion powder (containing less than 5 mg quercetin aglycone),
*neuroP↑, implying its great neuroprotective potentials in AD.65
*p‑tau↓, quercetin inhibited tau hyperphosphorylation in a cell model induced by okadaic acid
*GSK‐3β↓, through suppressing tau phosphorylationrelated kinases, such as GSK-3β and CDK5
*CDK5↓,
| - |
Review, |
Nor, |
NA |
|
|
|
- |
Review, |
IBD, |
NA |
|
|
|
*antiOx↑, Rutin is a highly potent molecule due to its strong antioxidant properties
*antiAll↑, antiallergic [21] , anti-inflammatory and vasoactive [22] , antitumor [23] , antibacterial, antiviral, and antiprotozoal properties
*Inflam↓,
*AntiTum↑,
*Bacteria↓,
*AntiViral↑,
*BioAv↓, The major disadvantage associated with this molecule is poor solubility in aqueous media, being the reason for its poor bioavailability.
*AntiArt↑, Antiarthritic activity
*PLA2↓, rutin inhibited PLA2 activity, the initial enzyme in arachidonic acid cascade, from human synovial fluid
*chemoP↑, Rutin pretreatment prevented deteriorative effects induced by cisplatin through a protective mechanism that involved reduction of increased oxidative stress as well as caspase-3, TNF-a and NF-kB protein expression levels.
*ROS↓,
*Casp3↓,
*TNF-α↓,
*NF-kB↓,
*cardioP↑, Recent studies have shown the protective effect of rutin in various cardiovascular disorders such as hypertension, hyperlipidemia and myocardial infarction
*Stroke↓, The protective effects of rutin in myocardial infarction could be due to free radical scavenging activity, improving of multienzyme activities such as Na + /K + ATPase and Mg 2+ -ATPase and Ca 2+ -ATPase
*TG/TAG↓, Rutin significantly lowered levels of cholesterol, TGs, free fatty acids (FFAs), LDL-C, and VLDL-C in serum and increased the level of HDL-C in serum in ISO-treated rats (
*FFA/NEFA↓,
*LDL↓,
*HDL↑,
*AntiDiabetic↑, Rutin acts as an antidiabetic agent in several ways by enhancing the release of insulin from islets of langerhans,
*MPO↓, Rutin has shown to be effective in treatment of IBD due to its anti-inflammatory effects, which involve reduction in myeloperoxidase activity and inhibition of TNF-a-induced NF-kB activation in human colon cells and expression of IL-1b
*NF-kB↓,
*BioAv↓, The oral bioavailability of pure rutin is around 20%
*BioAv↝, Common approaches used to enhance bioavailability of rutin are particle diminution to the submicron range and by complexation of rutin with cyclodextrins and various metals.
*antiOx↑, vitexin as an antioxidant against reactive oxygen species, lipid peroxidation, and other oxidative damages in a variety of oxidative stress‐related diseases,
*ROS↓, vitexin (10, 25, and 50 μM) dose‐dependently decreased ROS
*lipid-P↓,
*memory↑, including seizure, memory impairment, cerebral ischemia, neurotoxicity, myocardial and respiratory injury
*Stroke↓,
*cardioP↑, figure 2
*neuroP↑,
*Inflam↓,
*NRF2↑, Upregulation of antioxidant response genes (Nrf2, HO‐1, NQO‐1, and Grp78) Downregulated Gadd153
*HO-1↑,
*NQO1↑,
*GRP78/BiP↑,
*CHOP/DDIT3↓,
*BACE/β-secretase↓, (vitexin and quercetin 3‐O‐glucoside), isolated from Nelumbo nucifera embryos, showed a potent inhibitory activity against β‐site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) and Cholinesterase (ChE).
*ChE↓,
*AChE↓, Vitexin (100 µM) showed significant cholinesterase inhibitory effects for both acetylcholinesterase and butyrylcholinesterase activity
*BChE↓,
*GSH↑, vitexin could prevent the reduction of glutathione levels, the ferric‐reducing ability potential, and the free‐radical scavenger ability, inhibit the production of hyperalgesic cytokines, such as TNF‐α, IL‐1β, IL‐6, and IL‐33, and upreg
*TNF-α↓,
*IL1β↓,
*IL6↓,
*IL33↓,
*LDH↓, It also reduced LDH and CK activities and MDA level and increased SOD in the serum.
*MDA↓,
*SOD↑,
| - |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Var, |
NA |
|
|
|
*antiOx↑, antioxidant, anti-inflammatory, anticancer, antibacterial, and neuroprotective mechanisms.
*Inflam↓,
*AntiCan↑,
*Bacteria↓,
*neuroP↑, cardiovascular protection, blood sugar regulation, anti-obesity, anticancer, antioxidant, anti-inflammatory, and neuroprotective properties.
*Obesity↓,
*cardioP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*ROS↓, Sprague-Dawley rat hearts, H9c2 cells 10 μM Reducing ROS levels; improving mitochondrial activity, mitochondrial membrane potential, and ATP content; markedly increasing MFN2 expression and reducing the recruitment of Drp1 in mitochondria.
*MMP↑,
*ATP↑,
*MFN2↑,
*DRP1/DNM1L↓,
*FOXO3↑, Protect against DOX-induced acute cardiotoxicity Rats 30 mg/kg Vitexin induced elevated FOXO3a protein expression levels, by suppressing oxidative stress
*NRF2↑, vitexin activated nuclear factor-erythroid 2-related factor 2 (Nrf2) in HUVEC under high glucose.
*Ferroptosis↓, Diabetic nephropathy HK-2 cells/DN rat 0–40 μM Vitexin could alleviate diabetic nephropathy by attenuated ferroptosis via activating GPX4
*GPx4↑,
TumCP↓, Gastric cancer Nude mice/GC cells 2 mg/kg 10–160 μM Vitexin inhibited the malignant progression of GC in vitro and in vivo by suppressing HMGB1-mediated activation of PI3K/Akt/HIF-1α signaling pathway.
HMGB1↓,
PI3K↓,
Akt↓,
Hif1a↓,
CDK1↓, Colon cancer HCT-116 cells 1–300 μM Inhibit colon cancer HCT-116 cell proliferation by suppressing CDK1/cyclin B expression, leading to cell cycle arrest in the G2/M phase.
CycB/CCNB1↓,
TumCCA↑,
Apoptosis↑, Isovitexin Colon cancer Promoted apoptosis and suppressed cell proliferation by activating the p53 signaling pathway.
P53↑,
NF-kB↓, Non-small cell lung cancer cells A549/ H1299 cells, nude mice 1–120 μM Suppressed NF-κB, AKT and ERK activation. [24] Vitexin A549 cells, nude mice 0–40 μM Reduced the levels of p-PI3K, p-Akt, and p-mTOR.
ERK↓,
p‑PI3K↓,
miR-34a↑, Isovitexin Hepatocarcinoma SK-Hep-1 cells Mediated miR-34a upregulation induces apoptosis and suppresses the stemness of SK-SC.
Apoptosis↑,
CSCs?,
*MAPK↓, Isovitexin Acute lung injury RAW 264.7 cells 0–50 μM Inhibiting MAPK and NF-κB and activating HO-1/Nrf2 pathways.
*HO-1↑,
*hepatoP↑, EAH mice 5 mg/kg Vitexin ameliorated hepatic injury in EAH mice through activation of the AMPK/AKT/GSK-3β pathway and upregulation of the Nrf2 gene.
*AMPK↑,
*Akt↑,
*GSK‐3β↑,
*chemoP↑, Vitexin exerts a cardioprotective effect against DOX-induced cardiac toxicity by reducing oxidative stress, lowering cardiac inflammatory cytokines, increasing FOXO3a, and inhibiting caspase-3 activation.
*Casp3↓,
*IRes↝, Vitexin and isovitexin flavonoids not only affected the absorption of peripheral glucose in insulin and non-insulin sensitive tissues but also showed the potential to restore insulin resistance in HepG2 cells by enhancing cellular uptake of glucose.
*GlucoseCon↑,
ChemoSen↑, When combined with doxorubicin (Dox), vitexin can reduce tumor growth and show synergistic effects in in vivo tests, increasing antitumor efficacy.
*GSH↑, Vitexin also increased Nrf2 expression and boosted GSH and antioxidant enzymes such as SOD, CAT, GPx, and GST.
*SOD↑,
*ATF2↑,
*GPx↑,
*GSTs↑,
*AntiAge↑, In Caenorhabditis elegans, studies have shown that vitexin and isovitexin, as putative SKN-1/Nrf2 activators, increase lifespan and support a healthy lifespan.
*Stroke↓, It has been demonstrated that vitexin protects against a cerebral ischemia/reperfusion (I/R)-induced increase in the permeability of brain endothelial cells
*AChE↓, vitexin treatment significantly inhibited acetylcholinesterase activity and markedly downregulated the expression of ace-1 and ace-2.
*ACE/ACE1↓,
*ACE2↓,
*GutMicro↑, Vitexin and isovitexin have also shown promising potential in modulating intestinal microbiota and in turn play a significant role in regulating various diseases such as overweight
*MPO↓, Vitexin can also resist Helicobacter pylori infection, which may be related to its anti-myeloperoxidase (MPO) enzyme activity and inhibition of H- and K-ATPase activity
*H+/K+-ATPase↓,
*AntiDiabetic↑, Antidiabetic Vitexin and Isovitexin Inhibits α-glucosidase/α-amylase, promotes GLUT4, modulates gut microbiota
*GLUT4↑,
*Obesity↓, Anti-obesity Vitexin Activates AMPKα, inhibits C/EBPα, FAS, activates Hedgehog signaling
*HH↓,
*RenoP↑, vitexin protects the kidneys and prevents the formation of kidney stones by inhibiting pyroptosis, apoptosis, epithelial–mesenchymal transition (EMT), and macrophage activation.
*BioAv↓, Vitexin and isovitexin have poor absorption in the gastrointestinal tract, with significant first-pass effects in the intestine (approximately 94%), stomach (30%), and liver (50%), resulting in a lower bioavailability (F) (approximately 5%).
*BioAv↝, The absorption and metabolism processes of vitexin and isovitexin in the human body are complex, and their bioavailability is influenced by multiple factors, including the action of the gut microbiota, interactions with dietary components, first-pass
*BioAv↑, The vitexin-loaded bilayer nanoparticles are designed by assembling soybean peptides and coating them with a goblet cell-targeting peptide. They significantly increase the bioaccessibility and bioavailability of vitexin
Showing Research Papers: 1 to 33 of 33
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 33
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
ACE/ACE1↓, 1, BMP7/OP1↓, 1, CD47↓, 1, miR-124-3p↓, 1, MTA1↓, 1, PFS↑, 1, PLA2↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↓, 2, GSH↓, 2, MDA↑, 1, ROS↓, 1, ROS↑, 1, SOD↓, 2, TAC↓, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
Tf↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 2, PGC-1α↑, 1, XIAP↓, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
cMyc↓, 1, SCD1↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 5, p‑Akt↓, 1, Apoptosis↑, 6, BAD↑, 1, Bak↑, 1, BAX↑, 1, Bcl-2↓, 4, Bcl-xL↓, 2, Casp↑, 1, Casp3↑, 5, Casp8↑, 2, Casp9↑, 3, Cyt‑c↑, 2, Fas↑, 1, IAP1↓, 1, IAP2/BIRC3↓, 1, iNOS↓, 1, MAPK↓, 1, Mcl-1↓, 1, p27/CDKN1B↑, 1, survivin↓, 1, TumCD↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
EZH2↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, HSP90↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↑, 4,
DNA Damage & Repair(tgid=10) ⓘ
P53↓, 1, P53↑, 2, PARP↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK4↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, mitA↑, 1, TumCCA↑, 5,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs?, 1, ERK↓, 2, FOXO3↓, 1, GSK‐3β↑, 1, HDAC1↓, 1, miR-34a↑, 1, mTOR↓, 2, P70S6K↓, 1, PI3K↓, 4, p‑PI3K↓, 1, PTEN↑, 1, SHP1↑, 1, STAT↓, 1, STAT3↓, 2, TumCG↓, 1,
Migration(tgid=13) ⓘ
BACH1↓, 1, Ca+2↓, 1, LAMs↓, 1, LRP1↓, 1, MALAT1↓, 1, MMP2↓, 3, MMP9↓, 1, TIMP2↓, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 5, TumMeta↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, EGFR↓, 1, Hif1a↓, 4, VEGF↓, 3,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 3, HMGB1↓, 1, IL1β↓, 1, IL6↓, 2, IL8↓, 1, JAK1↓, 1, JAK2↓, 1, M2 MC↓, 1, NF-kB↓, 4, NK cell↑, 1, PD-1↓, 1, PD-L1↓, 1, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↝, 1, ChemoSen↑, 4, Dose↝, 4, eff↑, 4, selectivity↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 1, EZH2↓, 1, IL6↓, 2, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 3, AntiTum↑, 1, chemoP↑, 1, chemoPv↑, 1, NP/CIPN↓, 2, QoL↑, 1, radioP↑, 1, RenoP↑, 1, Risk↓, 1, TumVol↓, 2, TumW↓, 1,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 1, CD8+↑, 2,
Total Targets: 128
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
ACE/ACE1↓, 1, ACE2↓, 1, Airway↓, 1, AirwayM↓, 1, ALDOC↑, 1, antiAll↑, 1, AntiArt↑, 2, AntiBio↑, 2, antiD↓, 1, BALF-Infl↓, 1, BALF-Lym↓, 1, compII↑, 1, CXCL15↓, 1, Eos↓, 1, FFA/NEFA↓, 1, H+/K+-ATPase↓, 1, IL13↓, 1, IRes↝, 1, PAF↑, 1, PLA2↓, 1, Stroke↓, 33,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 1, antiOx↑, 10, Catalase↑, 4, Ferroptosis↓, 2, GPx↑, 3, GPx4↑, 2, GSH↑, 5, GSTs↑, 1, HDL↑, 1, HO-1↓, 1, HO-1↑, 6, hyperG↓, 1, i-Iron↓, 1, Keap1↓, 1, Keap1↝, 1, lipid-P↓, 3, MDA↓, 9, MFN2↑, 1, MPO↓, 6, NQO1↑, 1, NQO1↝, 1, NRF2↓, 1, NRF2↑, 9, ROS↓, 17, mt-ROS?, 1, SOD↑, 7, xCT/SLC7A11↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↓, 1, ATP↑, 3, compIII↑, 1, DRP1/DNM1L↓, 1, Insulin↑, 1, MMP↑, 3, mtDam↓, 1, PGC-1α↝, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACSL4↓, 1, AKT1↑, 1, ALAT↓, 4, AMPK↑, 1, BUN↓, 1, glucose↓, 1, GlucoseCon↑, 1, LDH↓, 1, LDH↑, 1, LDL↓, 2, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Akt↑, 2, p‑Akt↑, 2, Apoptosis↓, 4, ATF2↑, 1, BAX↓, 2, Bcl-2↑, 3, Casp1↓, 1, Casp12↓, 1, Casp3↓, 5, Ferroptosis↓, 2, GranB/GZMB↓, 1, iNOS↓, 2, p‑JNK↓, 1, MAPK?, 1, MAPK↓, 3, p38↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1, other?, 1, other↓, 1, other↑, 1, other↝, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↓, 2, p‑eIF2α↓, 1, ER Stress↓, 1, GRP78/BiP↓, 1, GRP78/BiP↑, 1, XBP-1↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1/ATG6↑, 1, LC3‑Ⅱ/LC3‑Ⅰ↑, 1, LC3II↑, 1, p62↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, PARP1↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
FOXO3↑, 1, GSK‐3β↓, 2, GSK‐3β↑, 2, p‑GSK‐3β↑, 1, HH↓, 1, mTOR↓, 2, p‑mTOR↑, 1, PI3K↓, 2, PI3K↑, 1,
Migration(tgid=13) ⓘ
AntiAg↓, 1, AntiAg↑, 1, APP↓, 1, BACH1↓, 1, CDK5↓, 1, PAI-1/SERPINE1↓, 1, TGF-β↑, 1, TIMP1↓, 1, VCAM-1↓, 2, ZO-1↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↑, 1, ATF4↓, 1, NO↓, 2, VEGF↑, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 2, BBB↝, 1, GLUT4↑, 1, IBI↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
ASC↓, 1, CD4+↑, 1, COX2/PTGS2↓, 3, COX2/PTGS2↑, 1, ICAM-1↓, 2, IFN-γ↓, 2, IL10↑, 1, IL18↓, 1, IL1β↓, 7, IL33↓, 1, IL4↓, 3, IL6↓, 8, IL8↓, 3, Imm↑, 2, Inflam↓, 18, LPS↓, 1, pol-M2 MC↑, 1, MCP1/CCL2↓, 2, MIP2↓, 1, Neut↓, 1, NF-kB↓, 7, PGE2↓, 2, RANTES↓, 1, TLR4↓, 1, TNF-α↓, 9,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↑, 1, AChE↓, 6, BChE↓, 2, BDNF↑, 2, BrainVol↑, 1, ChE↓, 1, NGF↑, 2, p‑tau↓, 3, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 2, Aβ↓, 4, BACE/β-secretase↓, 4, NLRP3↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 7, BioAv↑, 5, BioAv↝, 4, Dose?, 1, Dose↓, 1, Dose↑, 2, Dose↝, 8, eff↑, 6, Half-Life↓, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 4, AST↓, 5, BloodF↑, 1, BMD↑, 1, creat↓, 1, GutMicro↑, 3, IL6↓, 8, LDH↓, 1, LDH↑, 1, TG/TAG↓, 1, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 6, AntiDiabetic↑, 7, antiPs↑, 2, AntiTum↑, 2, cardioP↑, 11, chemoP↑, 3, cognitive↑, 6, hepatoP↑, 9, memory↑, 5, neuroP?, 1, neuroP↑, 21, Obesity↓, 6, RenoP↓, 1, RenoP↑, 5, Risk↓, 1, toxicity↓, 10,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↓, 1, AntiFungal↑, 1, AntiViral↑, 4, Bacteria↓, 6, Sepsis↓, 4,
Total Targets: 209
Scientific Paper Hit Count for: Stroke, Stroke
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1534 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
Home Page