neuroG Cancer Research Results
neuroG, neurogenesis: Click to Expand ⟱
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Neurogenesis is the process by which nervous system cells, the neurons, are produced by neural stem cells.
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Scientific Papers found: Click to Expand⟱
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*Inflam↓, results showed that CuB exhibits potent anti-inflammatory, antioxidant, antiviral, hypoglycemic, hepatoprotective, neuroprotective, and anti-cancer activities
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*AntiCan↑,
*toxicity↝, Studies of its toxicity and pharmacokinetic properties showed that CuB has non-specific toxicity and low bioavailability.
*BioAv↓,
*HO-1↑, CuB can exert its anti-inflammatory effect via the induction of heme oxygenase-1 (HO-1) by the activation Nrf2 [25].
*NRF2↑,
*NLRP3↑, CuB could act as an anti-inflammatory agent to inhibit gouty arthritis in mice [28]. The mechanism of action was mainly attributed to inhibition of the formation and activation of the NOD-like receptor thermal protein domain associated protein 3 (NLR
*SOD↑, Its antioxidant activity may be indirectly realized by increasing the activities of the antioxidant enzymes total SOD and SOD-1, and thereby eliminating excessive ROS and other free radicals in cells
*SOD1↑,
*ROS↓,
*AntiAge↑, this study also confirmed that CuB could exert anti-aging effects by regulating autophagy, ROS, and aging-related genes, which suggested that CuB might be a promising anti-aging drug
*ARE↑, activating the Nrf2/ARE signaling pathway and inhibiting the STAT/NF-κB signaling pathway, and thereby exerting a protective effect on cortical neurons
*STAT↓,
*NF-kB↓,
*neuroG↑, CuB (0.1 mg/kg) could also promote neurogenesis in APP/PS1 mice and alleviate memory deficits associated with enhanced neurogenesis in mice.
*memory↑,
ROS↑, Figure 2
NLRP3↑,
CIP2A↓,
Akt↓,
STAT3↑,
VEGFR2↓,
DNMTs↓, tudies have shown that in H1299 human lung cancer cells CuB (6, 60, 600, and 860 nM) can inhibit DNA methyltransferases (DNMTs)
MAPK↓,
YAP/TEAD↓,
PI3K↓,
Wnt↓,
NOTCH↓,
TumCCA↑,
TumCG↓, Inhibit cell growth and proliferation
TumCP↓,
FAK↑, CuB inhibited the migration, invasion, and adhesion of KKU-452 CCA cells in a dose-dependent manner by suppressing the activation of FAK and down-regulating MMP-9,
MMP9↓,
TumAuto↑, CuB ccould induce autophagy in BEL-7402 hepatocellular carcinoma cells by affecting autophagy-related proteins, such as up-regulating the expression of light chain 3 (LC3)-II
toxicity↝, Most experiments have demonstrated that CuB is moderately cytotoxic, both to human cancer cells and to normal cells
BioAv↓, When Wistar rats were given CuB orally at a dose of 8 mg/kg, the absorption degree was low and the absorption speed was slowest, which was specifically reflected in the fact that the time to peak concentration was longest (180 min, Tmax = 3 h). T
Half-Life↝, When CuB was administered intravenously at 0.1 mg/kg and orally at 1 mg/kg, the clearance rates of CuB in Wistar rats were similar, with a half-life (t1/2) of 5.08 ± 2.87 h and 5.09 ± 2.20 h, respectively [139].
BioAv↑, CuB-loaded mixed micelles with collagen peptides as a carrier, which improved the solubility of CuB and enhanced the absorption of orally administered CuB, and its relative bioavailability increased by a factor of 3.43
selectivity∅, Although CuB displays potent activity against tumor cells, its non-selective toxicity has limited its clinical applications.
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*AntiCan↑, gained increasing interest due to its proposed anti-cancer, anti-obesity, anti-inflammatory, antioxidant, and lipid-lowering effects, in addition to its thermogenic capacity.
*Obesity↓,
*Inflam↓,
*lipid-P↓,
*BioAv↓, intact curcumin in the body may be too low (<1 microM) and not sufficient to affect signaling and gene expression, as observed in vitro with cultured cells (10–20 microM).
*BioAv↑, a myriad of nanoformulations have been developed that either lead to a systemic increase in curcumin or are targeted to specific cells, tissues, or organelles
*BioAv↑, latest generation of curcumin nanoformulations can increase the bioavailability of free curcumin in plasma greater than 100-fold and have superior absorption, cellular uptake, BBB permeability, and tissue distribution
*BioAv↑, In a clinical study, the authors found that 2 g of curcumin administered concomitantly with 20 mg of piperine, an inhibitor of hepatic and intestinal glucuronidation, appeared to promote a significant 2000% increase in the oral bioavailability of cur
*BioAv↑, rats in which piperine pre-administration was performed before receiving curcumin, there was a significant increase in the oral bioavailability of curcumin, especially at 6 h after piperine administration
*BioAv↑, Nanotechnology-based delivery systems such as micelles, liposomes, and polymeric, metal, and solid lipid nanoparticles have also been applied to enhance curcumin bioavailability
*ROS↓, Curcumin was effective against ischemia/reperfusion (I/R) lesions, as well in various experimental models, primarily through antioxidant actions such as scavenging ROSs [153], increasing mitochondrial superoxide dismutase (SOD) activity and decreasin
*mt-SOD↑,
*MDA↓,
*BBB↓, Curcumin has poor bioavailability, especially in the brain, where the BBB further limits its absorption
*Aβ↓, curcumin appears to reduce the production of Aβ also by affecting a second enzyme required for the cleavage of APP
*GSK‐3β↓, the inhibition of GSK3β by curcumin would hinder both Aβ production and tau aggregation
*tau↓,
*neuroG↑, prolonged treatment of aged rats with curcumin stimulates neurogenesis in the hippocampus
*memory↑, chronic curcumin administration improved memory acquisition and consolidation in both adult and aged rats
cardioP↑, curcumin has been investigated to promote cardioprotective effects against chemotherapy-induced cardiotoxicity
*angioG↑, angiogenic and neuroprotective effects of EGCG
*neuroG↑,
*NRF2↑, via upregulation of Nrf2 signaling pathway.
*neuroP↑, Exercise is known to have numerous neuroprotective and cognitive benefits, especially pertaining to memory and learning related processes.
*cognitive↑,
*memory↑,
*BDNF↑, relationship between exercise and hippocampal neurogenesis, and identifies a key molecule mediating this process, brain-derived neurotrophic factor (BDNF).
*neuroG↑, brain-derived neurotrophic factor (BDNF), that has been shown to modulate neurogenesis and how exercise influences BDNF levels
*BDNF↑, provide novel evidence that luteolin treatment, by restoring microglia alterations and transiently boosting BDNF/TrkB signaling
*Mood↑, Treatment with Luteolin Ameliorates Behavioral Deficits in Cdkl5 +/− Mice
*neuroG↑, Treatment with Luteolin Promotes Neurogenesis in the Hippocampus of Cdkl5 +/− Mice
*TrkB↑, Treatment with Luteolin Transiently Boosts BDNF/TrkB Signaling Pathways in the Cortex of
Cdkl5 +/− Mice
*neuroG↑, 2 weeks of naringin supplementation may have protective effects on impaired neurogenesis and BDNF levels after brain ischemia and reperfusion in rats
*BDNF↑,
*motorD↑, Naringin Improved Motor Function After Ischemia/Reperfusion
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*BBB↑, SF is able to cross the blood–brain barrier as well as to protect it
*BDNF↑, SF can protect against neuronal cell death by inhibiting apoptosis, by upregulating brain-derived neurotrophic factor (BDNF) it can enhance neuronal function and plasticity, and support neurogenesis.
*neuroG↑,
*NRF2↑, , Nrf2 inducers like SF that have no direct redox activity are often referred to as “indirect antioxidants”
*HO-1↑, (NQO1) (HO-1 or HMOX), as well as (Cat), (SOD), (Prx), (HSP), glutathione S-transferases (GST), thioredoxin reductase (Trx), glutathione synthetase (GS), glutathione peroxidases (GPx) and glutathione reductase in the brain
*Catalase↑,
*SOD↑,
*HSPs↑, It enhances the expression of HSP70, HSP90, and HSP40 in normal human fibroblasts
*GSTs↑,
*Trx↑,
*GPx↑,
*GSR↑,
*GSH↑, ability of SF to upregulate GSH in the brain is critical for antioxidant protection in youth but may become even more important with age.
*NQO1↑, SF administration to astrocytes increased NQO1 concentrations and protected against oxygen and glucose-induced astrocyte cell death
*GutMicro↑, the fact that SF modulates microbiome composition
*Inflam↓, reduces inflammation and enhances gut barrier integrity,
*neuroP↑, The effect of SF on the gut microbiome may also affect the production of short-chain fatty acids (SCFA) like butyrate, which have neuroprotective effects
*Hif1a↑, TQ can activate the HIF-1α pathway and its downstream genes such as VEGF, TrkB, and PI3K, which in turn enhance angiogenesis and neurogenesis.
*VEGF↑,
*TrkB↑,
*PI3K↑,
*angioG↑, which in turn enhance angiogenesis and neurogenesis.
*neuroG↑,
*motorD↑, TQ has the same effect as DMOG to activate HIF-1 α and can improve motor dysfunction after ischemic stroke
*cognitive↑, UA ameliorated cognitive impairment, prevented neuronal apoptosis, and enhanced neurogenesis in APP/PS1 mice.
*Apoptosis↓,
*neuroP↑,
*Aβ↓, UA attenuated Aβ deposition and peri-plaque microgliosis and astrocytosis in the cortex and hippocampus.
*AMPK↑, enhancing cerebral AMPK activation, decreasing the activation of P65NF-κB and P38MAPK, and suppressing Bace1 and APP degradation.
*NF-kB↓,
*MAPK↓,
*BACE↑,
*neuroG↑, triggering neurogenesis via anti-inflammatory signaling in APP/PS1 mice,
*Inflam↓,
*memory↑, UA ameliorates learning and memory deficits in APP/PS1 mice
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*MitoP↓, Experimental models consistently show that UA increases mitophagy and mitochondrial function and blunts excessive inflammatory responses.
*Strength↑, UA is a promising strategy to target health and disease conditions of aging, especially those linked to mitochondrial and muscle dysfunction.
*PINK1↑, UA can activate. PTEN-induced kinase 1 (PINK1)/Parkin-dependent mitophagy starts with the stabilization of the kinase PINK1,
*PARK2↑, which recruits and phosphorylates the ubiquitin-conjugating protein Parkin.
*Inflam↓, anti-inflammatory effect of UA was reported for the first time as a decrease in mRNA and protein levels of the inflammatory marker cyclooxygenase 2 (COX2)
*COX2↓,
*IL1β↓, In neuronal tissues, UA treatment reduced levels of IL-1β, IL-6, and TNFα in the brains of the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD
*IL6↓,
*TNF-α↓,
*OS↑, impact on worm longevity showed that UA extends lifespan by 45%,
*cardioP↑, reduction in IRI markers, such as circulating creatine kinase and lactate dehydrogenase levels, and by fewer apoptotic cells in the heart
*memory↑, Increased learning, memory retention, neuronal survival, and neurogenesis in the hippocampus was achieved with UA administration in the APP/PS1 mouse model of AD
*neuroG↑,
*neuroP↑, UA was shown to have neuroprotective effects in the EAE mouse model of multiple sclerosis (MS)
*Cartilage↑, In a model of osteoarthritis, an age-related and disabling joint disease caused by a slow degeneration of cartilage,
*Inflam↓, UA has protective effects against a chronic DSS-induced model of IBD, leading to reduced levels of colon inflammation markers and to better mucosal integrity.
*RenoP↑, UA consistently reduced tubular damage induced by cisplatin, as shown by histopathology and by a reduction in circulating markers of kidney damage
*eff↑, When administered as nanoparticles to increase its bioavailability, UA even improved the survival of mice that received a lethal dose of cisplatin
*Dose↝, UA showed a favorable safety profile, with no observed side effects following either single oral administration of UA up to 2000 mg or multiple oral dosing (28 days) of UA up to 1000 mg daily.
*Half-Life↑, It showed a relatively long-half life (t1/2 = 17–22 hours),
*NRF2↑, Other mechanisms of action have been proposed for UA, such as the activation of the Ahr/Nrf2 pathway and its downstream antioxidative stress response
*GutMicro↑, A recent report also showed an impact of direct UA supplementation on gut microflora in obese rats
*memory↑, Urolithin A (Uro-A), a type of polyphenol derived from pomegranate, is known to improve memory function when ingested
*SIRT1↑, through the activation of longevity gene SIRT1.
*cognitive↑, therapeutic potential of Uro-A for cognitive health.
*BDNF↑, enhanced expression of several intestine-derived secretory factors, including BDNF, NT-4, (Figure S2), and ciliary neurotrophic factor (CNTF)
*Apoptosis↓, Uro-A prevents neuronal apoptosis and enhances neurogenesis, thereby inhibiting cognitive impairment in model mice
*neuroG↑,
*antiOx↑, Pomegranate (Punica granatum L.), is one such fruit that is well known for its medical usage due to its antioxidant properties.
*neuroG↑, pomegranate supplementation has been shown to impart cognitive aid by the protection of neurons and triggering neurogenesis through anti-inflammatory signaling pathway.
*Inflam↓,
*cognitive↑,
*neuroP↑, deficiency impairs memory and learning in AD. RA acts as a neuroprotective agent by regulating gene expression, and neuronal survival
memory↑,
*Inflam↓, VA deficiency is also associated with elevated inflammatory cytokines, promoting neuroinflammation involved in AD progression
*neuroG↑, RA also stimulates adult neurogenesis, potentially influencing cognition in AD [17].
*cognitive↑,
*Aβ↓, It also influences Aβ clearance and tau phosphorylation, key pathological features of AD [19].
p‑tau↓,
*BACE↓, VA deficiency enhances BACE1 activity, increasing Aβ production and promoting neurotic plaque formation, a hallmark of AD pathology [21]
Showing Research Papers: 1 to 13 of 13
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↑, 1,
Cell Death ⓘ
Akt↓, 1, MAPK↓, 1, YAP/TEAD↓, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNMTs↓, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
CIP2A↓, 1, NOTCH↓, 1, PI3K↓, 1, STAT3↑, 1, TumCG↓, 1, Wnt↓, 1,
Migration ⓘ
FAK↑, 1, MMP9↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature ⓘ
VEGFR2↓, 1,
Synaptic & Neurotransmission ⓘ
p‑tau↓, 1,
Protein Aggregation ⓘ
NLRP3↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 1, Half-Life↝, 1, selectivity∅, 1,
Functional Outcomes ⓘ
cardioP↑, 1, memory↑, 1, toxicity↝, 1,
Total Targets: 26
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, ARE↑, 1, Catalase↑, 1, GPx↑, 1, GSH↑, 1, GSR↑, 1, GSTs↑, 1, HO-1↑, 2, lipid-P↓, 1, MDA↓, 1, NQO1↑, 1, NRF2↑, 4, PARK2↑, 1, ROS↓, 2, SOD↑, 2, mt-SOD↑, 1, SOD1↑, 1, Trx↑, 1,
Mitochondria & Bioenergetics ⓘ
PINK1↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Apoptosis↓, 2, MAPK↓, 1,
Protein Folding & ER Stress ⓘ
HSPs↑, 1,
Autophagy & Lysosomes ⓘ
MitoP↓, 1,
Proliferation, Differentiation & Cell State ⓘ
GSK‐3β↓, 1, neuroG↑, 13, PI3K↑, 1, STAT↓, 1,
Migration ⓘ
Cartilage↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 2, Hif1a↑, 1, VEGF↑, 1,
Barriers & Transport ⓘ
BBB↓, 1, BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 8, NF-kB↓, 2, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
BDNF↑, 5, tau↓, 1, TrkB↑, 2,
Protein Aggregation ⓘ
Aβ↓, 3, BACE↓, 1, BACE↑, 1, NLRP3↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 5, Dose↝, 1, eff↑, 1, Half-Life↑, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 2, IL6↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiCan↑, 2, cardioP↑, 1, cognitive↑, 5, hepatoP↑, 1, memory↑, 6, Mood↑, 1, motorD↑, 2, neuroP↑, 6, Obesity↓, 1, OS↑, 1, RenoP↑, 1, Strength↑, 1, toxicity↝, 1,
Total Targets: 69
Scientific Paper Hit Count for: neuroG, neurogenesis
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
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