Inflam Cancer Research Results

Inflam, inflammation: Click to Expand ⟱
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Cancer and inflammation are closely linked, with chronic inflammation contributing to the development and progression of cancer. Various inflammatory mediators and cells are involved in this process.
Scientific Papers found: Click to Expand⟱
5425- ASTX,    Multiple roles of fucoxanthin and astaxanthin against Alzheimer's disease: Their pharmacological potential and therapeutic insights
- in-vivo, AD, NA
*neuroP↑, fucoxanthin and astaxanthin, natural carotenoids abundant in algae, has shown to possess neuroprotective properties through antioxidant, and anti-inflammatory characteristics in modulating the symptoms of AD.
*antiOx↑,
*Inflam↑,
*AChE↓, Fucoxanthin and astaxanthin exhibit anti-AD activities by inhibition of AChE, BuChE, BACE-1, and MAO, suppression of Aβ accumulation.
*BACE↓,
*MAOA↓,
*Aβ↓,
*memory↑, Recently, Che, Li (Che et al., 2018) reported that astaxanthin possessed memory enhancement.
*MDA↓, Astaxanthin, as an antioxidant, helps to reduce oxidative stress by lowering malondialdehyde (MDA) levels and increasing SOD activity by activation of the NrF2/HO-1 pathway
*SOD↑,
*NRF2↑,
*HO-1↑,
*NF-kB↓, astaxanthin showed NFκB inhibitory activity which caused the downregulation of BACE-1 expression, resulting in Aβ reduction
*GSK‐3β↓, astaxanthin dose-dependently attenuated the GSK-3β activity
*ChAT↑, astaxanthin could reduce neuroinflammation via reducing iNOS expression and spine loss on the hippocampal CA1 pyramidal neurons, and restoring the ChAT expression in the medial septal nucleus
*iNOS↓,
*ROS↓, astaxanthin treatment decreased the ROS production and enhanced the cell growth.
*BBB↑, Astaxanthin can attenuate neurological dysfunction because of its unique chemical structure and can cross the BBB to enter the brain tissue

5768- CAPE,    Neuroprotective Potential of Caffeic Acid Phenethyl Ester (CAPE) in CNS Disorders: Mechanistic and Therapeutic Insights
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*antiOx↑, it possesses antioxidant, anti-inflammatory, antimitogenic, and anti-cancer activities, as shown by preclinical studies.
*Inflam↑,
*AntiCan↑,
*NRF2↑, figure 1
*GSK‐3β↑,
*Akt↑,
*PI3K↑, directly activates the PI3/Akt signaling pathway as well as leads to increased phosphorylation of GSK-3β to yield it inactive
*ROS↓, decrease in the reactive oxygen species levels (ROS)
*SOD↑,
*GSH↑,
*MDA↓,
*tau↓, reduced hyperphosphorylation of Tau protein
*neuroP↑, Accorded neuroprotection through increased PI3K activity and eNOS mediated nitric oxide synthesis
*memory↑, CAPE treatment in the doses of 6 mg/kg for 28 days led to an improvement in spatial memory and reduction in the malondialdehyde (MDA),
*AChE↓, Other mechanisms which may contribute to its beneficial effect include the inhibition of acetylcholinesterase activity, which has also been reported by several authors
*other↝, Different studies have demonstrated the effectiveness of CAPE in stroke models through its anti-inflammatory and antioxidant properties.
*lipid-P↓, decreasing membrane fluidity, lipid peroxidation, release of cardiolipin, and Cyt c

5896- CAR,  TV,    Carvacrol and Thymol Hybrids: Potential Anticancer and Antibacterial Therapeutics
- Review, Var, NA
BioAv↑, hybrid compounds containing their pharmacophores to enhance their therapeutic efficacy and improve their bioavailability.
AntiCan↑, figure 2
*antiOx↑,
*Inflam↑,
*Bacteria↓,
ROS↑, they produce more reactive oxygen species (ROS), which interrupt the DNA of cancer cells
DNAdam↑,

5898- CAR,    Carvacrol-induced apoptosis via tumor suppressor gene activation and oxidative stress modulation in a rat model of breast cancer
- in-vivo, BC, NA
*lipid-P↓, Carvacrol also attenuated lipid peroxidation by reducing malondialdehyde (MDA) levels, while boosting total antioxidant capacity and improving inflammatory status.
*MDA↓,
*antiOx↑,
*Inflam↑,
RenoP↑, Moreover, restoration of liver and kidney function was observed through normalization of serum ALT, AST, urea, and creatinine levels
hepatoP↑,
*ALAT↓,
AST↓,
creat↓,
chemoPv↑, Preclinical studies have demonstrated the chemopreventive and therapeutic potential of Carvacrol in several malignancies, including breast cancer, melanoma, hepatocellular carcinoma, cervical cancer, and non-small cell lung cancer
Cyt‑c↑, markedly enhanced cytochrome c expression
FADD↑, . Carvacrol-injected therapy markedly elevated FADD expression
P53↑, Carvacrol receiving rat’s up-regulated P53 concentrations markedly that reached their peak in the injected (## P ≤ 0.01 vs. tumor and **P ≤ 0.01 vs. normal) as well as oral and mixed groups

6108- Chol,    Trimethylamine-N-Oxide (TMAO) as a Rising-Star Metabolite: Implications for Human Health
- Review, Nor, NA - Review, AD, NA
*TMAO↑, The gut microbiota’s role in metabolizing phytoestrogens suggests that these compounds can modulate the microbial community structure, potentially affecting the production of TMAO from dietary choline and carnitine [5].
*ROS↑, TMAO has the ability to induce oxidative stress in cells by promoting the production of reactive oxygen species (ROS).
*NADPH↑, TMAO has been shown to increase the activity of NADPH oxidase [30], an enzyme that generates ROS as part of its normal function.
*Ca+2↑, TMAO enters platelets and facilitates the release of calcium ions (Ca2+) from intracellular stores.
*AntiAg↓, Calcium serves as a critical secondary messenger in platelet activation, and its elevated levels promote platelet aggregation and thrombus formation
*cognitive↓, TMAO has been linked to cognitive decline and neurodegenerative disorders, including Alzheimer’s disease (AD). Through an integrated analysis of genetic, epigenetic, pathological, and biochemical data, Xu et al. identified a correlation between gut m
*TJ↓, However, excessive TMAO concentrations disrupt BBB integrity by inhibiting tight junction proteins, including claudin-5 and zonula occludens-1
*CLDN1↓,
*ZO-1↓,
*Inflam↑, TMAO also triggers neuroinflammation by activating the NLRP3 inflammasome,
*NLRP3↑,
*ER Stress↑, TMAO enhances the ER stress response by activating the PERK-eIF2α pathway, which is known to impair synaptic plasticity and neuronal function, processes strongly implicated in AD progression
*cognitive↓, TMAO has been identified as the most predictive biomarker for memory impairment and cognitive decline among 56 microbiota-derived metabolic markers
*Dose↝, use of cooking methods such as boiling or stewing instead of grilling, which can produce higher amounts of TMAO
*eff↑, Studies suggest that Lactobacillus plantarum ZDY04 could help reduce TMAO concentrations and prevent TMAO-induced atherosclerosis in animal models
*other↝, Currently, no medications specifically designed to reduce blood TMAO levels exist
*other↝, a review published in 2025 has highlighted the potential role of statins in lowering TMAO levels independently of their cholesterol-lowering effects
*other↝, scientific evidence suggests that statins selectively inhibit the growth of pathogenic bacteria, such as Clostridium and Ruminococcus, while promoting beneficial species, such as Bifidobacterium and Lactobacillus

3891- Cin,    Identification of potential targets of cinnamon for treatment against Alzheimer's disease-related GABAergic synaptic dysfunction using network pharmacology
- Analysis, AD, NA
*BBB↑, 17 components had a good absorption due to the blood–brain barrier (BBB) limitation;
*GABA↑, further clustering analysis of active ingredient targets by network pharmacology showed that the GABA pathway with GABRG2 as the core target was significantly enriched;
*eff↑, we screened five components, methyl cinnamate, propyl cinnamate, ( +)-procyanidin B2, procyanidin B1, and myristicin as the brain synapse-targeting active substances of cinnamon
*antiOx↑, Cinnamon is multi-targeted and multi-effective and is widely used in treating AD because of its antioxidant, anti-inflammatory, antibacterial, anti-anxiety and antidepressant properties
*Inflam↑,
*Mood↑,

6177- Cu,    Toxicity of copper oxide nanoparticles: a review study
- Review, Nor, NA
*ROS↑, The literature evidences that the CuO NPs exposure to the living systems results in reactive oxygen species generation, oxidative stress, inflammation, cytotoxicity, genotoxicity and immunotoxicity.
*Inflam↑,
*toxicity↑,
lipid-P↑, A549 cells that leads to high level of lipid peroxidation and ROS production while lower level of antioxidant (GSH) in HepG2
GSH↓,
MDA↑, They observed that MDA, a lipid peroxidation marker and antioxidant enzymes like SOD and CAT significantly increased followed by reduction in GSH level
*SOD↓, Lower level of GSH and inhibition of SOD and CAT activities by CuO NPs contributing to oxidative damages was also observed in embryo and while change in zebrafish physiology
*Catalase↓,

4826- CUR,    The Bright Side of Curcumin: A Narrative Review of Its Therapeutic Potential in Cancer Management
- Review, Var, NA
*antiOx↑, Curcumin demonstrates strong antioxidant and anti-inflammatory properties, contributing to its ability to neutralize free radicals and inhibit inflammatory mediators
*Inflam↑,
*ROS↓,
Apoptosis↑, Its anticancer effects are mediated by inducing apoptosis, inhibiting cell proliferation, and interfering with tumor growth pathways in various colon, pancreatic, and breast cancers
TumCP↓,
BioAv↓, application is limited by its poor bioavailability due to its rapid metabolism and low absorption.
Half-Life↓,
eff↑, curcumin-loaded hydrogels and nanoparticles, have shown promise in improving curcumin bioavailability and therapeutic efficacy.
TumCCA↑, Studies have demonstrated that curcumin can suppress the proliferation of cancer cells by interfering with the cell cycle [21,22]
BAX↑, Curcumin enhances the expression of pro-apoptotic proteins such as Bax, Bak, PUMA, Bim, and Noxa and death receptors such as TRAIL-R1/DR4 and TRAIL-R2/DR5
Bak↑,
PUMA↑,
BIM↑,
NOXA↑,
TRAIL↑,
Bcl-2↓, curcumin decreases the levels of anti-apoptotic proteins like Bcl-2, Bcl-XL, survin, and XIAP
Bcl-xL↓,
survivin↓,
XIAP↓,
cMyc↓, This shift in the balance of apoptotic regulators facilitates the release of cytochrome c from mitochondria [33,35] and activates caspases
Casp↑,
NF-kB↓, Curcumin suppresses the activity of key transcription factors like NF-κB, STAT3, and AP-1 and interferes with critical signal transduction pathways such as PI3K/Akt/mTOR and MAPK/ERK.
STAT3↓,
AP-1↓,
angioG↓, curcumin inhibits angiogenesis and metastasis by downregulating VEGF, VEGFR2, and matrix metalloproteinases (MMPs).
TumMeta↑,
VEGF↓,
MMPs↓,
DNMTs↓, Epigenetic modifications through the inhibition of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) further contribute to its anticancer properties.
HDAC↓,
ROS↑, curcumin-loaded nanoparticles showed significant cytotoxicity in the SCC25, MDA-MB-231, and A549 cell lines, with a decrease in tumor cell proliferation, an increase in ROS, and an increase in apoptosis.

6324- Eug,    Pharmacodynamic, pharmacokinetic, toxicity, and recent advances in Eugenol's potential benefits against natural and chemical noxious agents: A mechanistic review
- Review, Var, NA
*Inflam↑, EUG possesses notable anti-inflammatory, antioxidant, analgesic, antibacterial, antispasmodic, and apoptosis-promoting properties
*antiOx↑,
*Apoptosis↑,

6323- Eug,    Eugenol: An Insight Into the Anticancer Perspective and Pharmacological Aspects
- Review, Var, NA - Review, Arthritis, NA
*AntiCan↑, (Eug), a volatile phenolic bioactive compound with a formula of C10H12O2, has been reported to have anticancer, antidiabetic, cardio‐ and pulmonary protective roles.
*AntiDiabetic↑,
*cardioP↑, Eugenol has been proven effective in modulating gut microbiota and attenuating adiposity in high‐fat diet‐fed C57BL/6J mice.
*toxicity↝, According to WHO, the safe dose of eugenol is 2.5 mg/kg for consumption
*GutMicro↑,
*neuroP↑, Moreover, it has the ability to improve gut health and prevent neurodegenerative disorders.
*BioAv⇅, Furthermore, multiple carriers like liposomes, glycodendritic polyamine dextran, solid lipid nanoparticles, and corn protein nanoparticles have been reported to deliver eugenol.
*BioAv↝, Eugenol (150 mg) in gelatin capsules was orally administered in healthy adults and absorbed very quickly, and ~55% is eliminated in urine after being transformed to glucuronic acid or eugenol sulfate conjugate in the liver
*antiOx↑, The studies on eugenol have proved its antioxidant and anti‐inflammatory properties.
*Inflam↑,
*AntiArt↑, aMateen et al. (2019) reported that eugenol alleviated arthritis via attenuating pro‐inflammatory cytokines (TNF‐α, IL‐6, IL‐10).
*TNF-α↓,
*IL6↓,
*IL10↓,
*GSH↑, Eugenol (2.5, 5, 10 mg/kg) improved GSH, GPx, and CAT levels while reducing carrageenan‐induced OS in arthritic rats (Adefegha et al. 2019).
*GPx↑,
*Catalase↑,
*MDA↓, reported reduced MDA and improved SOD, CAT, and TAC levels.
*TAC↑,
TumCMig↓, eugenol subdued cell migration and invasion by suppressing angiogenesis‐related protein expression and modulating JAK2/STAT3 pathways.
TumCI↓,
Akt↑, MDA‐MB‐231, SK‐BR‐3 ↑AKT, FOXO3a, Caspase‐3/9, p21
FOXO3↑,
Casp3↑,
Casp9↑,
P21↑,
angioG↓, Eugenol has been reported to reduce angiogenesis, inhibit invasion, and trigger apoptosis
TumCI↓,
Apoptosis↑,
NF-kB↓, GC via apoptosis induction, metastasis inhibition, downregulation of NF‐κB, and angiogenesis reduction is shown in Figure 3
eff↑, eugenol (153 μM) combined with 5‐fluorouracil proved effective in inhibiting cell growth and division in HeLa cells.
eff↑, eugenol (200–350 μM) with sulforaphane (6.5–8 μM) lowered the expressions of COX‐2, IL‐β, and Bcl‐2 and inhibited cell proliferation
ChemoSen↑, co‐treatment of eugenol and cisplatin reduced cell proliferation and induced apoptosis in G361 melanoma cells via inhibited MMP and proteasome activity,
NA↑, Eugenol proved effective in HL‐60 cell lines by inducing ROS‐mediated apoptosis with a 23.7 IC50 value
Casp3↑, eugenol‐induced apoptosis via ROS production and caspase‐9/3 activation.
Casp9↑,
*AntiDiabetic↑, Chilukoti et al. (2024) verified the antidiabetic activity of eugenol in rats.
*glucose↓, eugenol (400 mg/kg) significantly lowered glucose levels, reduced OS and inflammation, inhibited MDA levels, and improved GSH.
*ROS↓,
*Inflam↓,
*MDA↓,
*GSH↑,
*BioAv↑, Multiple delivery systems, such as liposomes, nanoparticles, nanoemulsions, and hydrogels, enhance its bioavailability, controlled release, and targeted delivery, making eugenol more effective for pharmaceutical and biomedical applications.

1773- GA,    Impact of Gallic Acid on Gut Health: Focus on the Gut Microbiome, Immune Response, and Mechanisms of Action
- Review, Var, NA
antiOx↑, GA has many biological properties, including antioxidant, anticancer, anti-inflammatory, and antimicrobial properties.
AntiCan↑,
Inflam↑,
GutMicro↑, GA and its derivatives not only enhance gut microbiome (GM) activities, but also modulate immune responses
BioAv↝, polyphenols have high instability to light, heat, and pH due to the existence of multiple hydroxyl groups
BioAv↓, the poor solubility characteristics limit their wide application in the fields of food products and supplements
BioAv↑, Fortunately, the developing colloidal delivery systems could significantly improve its bioavailability, which brings large possibility for application in human.
TumMeta↓, gastric adenocarcinoma cell metastasis was inhibited by GA,

2521- H2,    Oxyhydrogen Gas: A Promising Therapeutic Approach for Lung, Breast and Colorectal Cancer
- Review, CRC, NA - Review, Lung, NA - Review, BC, NA
Inflam↑, Oxyhydrogen gas, a mixture of 66% molecular hydrogen (H2) and 33% molecular oxygen (O2) has shown exceptional promise as a novel therapeutic agent due to its ability to modulate oxidative stress, inflammation, and apoptosis.
ROS↓, neutralises reactive oxygen and nitrogen species
ChemoSen↑, enhancing existing treatments and reducing harmful oxidative states in cancer cells. boosting the effectiveness of conventional therapies
p‑PI3K↓, inhibiting the PI3K/Akt phosphorylation cascade.
p‑Akt↓,
QoL↑, Similar results have been observed in breast cancer, where patients reported improved quality of life.
GutMicro↑, improves intestinal microflora dysbiosis.
chemoP↑, reduced oxidative stress and mitigated tissue damage, suggesting its potential as a cytoprotective agent in cancer patients undergoing radiation therapy or chemotherapy
radioP↑,
*NRF2↑, documented role in activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.
*Catalase↑, consequently, hydrogen can enhance the expression of endogenous antioxidant enzymes, including catalase (CAT), glutathione peroxidase (GPx), haem oxygenase (e.g., HO-1), and superoxide dismutase (SOD) [45]
*GPx↑,
*HO-1↑,
*SOD↑,
*TNF-α↓, reducing the expression of proinflammatory mediators such as chemokines (e.g., CXCL15), cytokines (e.g., TNF-α), interleukins (e.g., IL-4, IL-6)
*IL4↓,
*IL6↓,
ChemoSen↑, further research demonstrates that oxyhydrogen gas enhanced the sensitivity of lung cancer cells to chemotherapy drugs, suggesting its potential as an adjuvant therapy
Appetite↑, inhaled oxyhydrogen gas over a minimum of 3 months. The results indicated substantial improvements in appetite, cognition, fatigue, pain, and sleeplessness
cognitive↑,
Pain↓,
Sleep↑,
other?, It is recommended that hydrogen should not exceed 4.6% in air or 4.1% by volume in pure oxygen gas (explosion risk)

4528- MAG,    Pharmacology, Toxicity, Bioavailability, and Formulation of Magnolol: An Update
- Review, Nor, NA
*Inflam↑, already known anti-inflammatory, cardiovascular protection, antiangiogenesis, antidiabetes, hypoglycemic, antioxidation, neuroprotection, gastrointestinal protection, and antibacterial activities of MG.
*cardioP↑,
*angioG↓,
*antiOx↑,
*neuroP↑,
*Bacteria↓,
AntiTum↑, Antitumor Activity
TumCG↓, MG suppressed the growth, migration, and invasion of tumor cells and promoted apoptosis
TumCMig↓,
TumCI↓,
Apoptosis↑,
E-cadherin↑, In MCF-7 cells, MG (20 μM) increased the expression of the tumor suppressor miRNA miR-200c to inhibit zinc finger E-box-binding homeobox 1 and increased the expression of E-cadherin
NF-kB↓, regulated the NF-κB pathway, induced cell cycle arrest, downregulated cyclin D1, and inhibited the expression of proliferating cell nuclear antigen (PCNA), Ki67, matrix metalloproteinase (MMP)-2, MMP-7, and MMP-9
TumCCA↑,
cycD1/CCND1↓,
PCNA↓,
Ki-67↓,
MMP2↓,
MMP7↓,
MMP9↓,
TumCG↓, A549 cells, MG (1–50 μM) showed growth inhibition and autophagy via activating caspase-3 and poly-(ADP)-ribose polymerase cleavage, reducing NF-κB/Rel A and Akt/mTOR pathway expression, dose-dependently blocking mitosis and G2/M progression, and incr
Casp3↑,
NF-kB↓,
Akt↓,
mTOR↓,
LDH↓,
Ca+2↑, MG (20–100 μM) played roles of [Ca2+] increase,
eff↑, cotreatment with MG and honokiol exerted a synergistic antitumor effect to induce cell cycle arrest as well as autophagy and inhibit proliferation by decreasing cyclin A/D1, cyclin-dependent kinase 2, 4, 6, p-PI3K, p-Akt, Ki67, p-p38, and p-JNK and
*toxicity↓, In summary, MG was found to be fairly nontoxic.
*BioAv↝, In recent years, the bioavailability of MG has been significantly improved by various formulations including solid dispersion, phospholipid complex, nanoparticles, emulsion, mixed micelles
*PGE2↓, exert neuroprotective activities by inhibiting the production of PGE2, regulating (GABA)A receptor subtypes
*TLR2↓, MG inhibited TLR2/TLR4/NF-κB/MAPK/PPAR-γ pathways and decreased the expression of inflammatory cytokines to exhibit anti-inflammatory activity.
*TLR4↓,
*MAPK↓,
*PPARγ↓,

1775- MEL,  Chemo,  Rad,    A Systematic Review of the Chemo/Radioprotective Effects of Melatonin against Ototoxic Adverse Effects Induced by Chemotherapy and Radiotherapy
- Review, Var, NA
chemoP↑, According to the findings, it was shown that melatonin co-treatment alleviates the ototoxic damage induced by chemotherapy and radiotherapy
radioP↑,
antiOx↑, melatonin may exert its otoprotective effects via its anti-oxidant, anti-apoptotic, and anti-inflammatory activities and other mechanisms.
Inflam↑,

2035- PB,    Sodium Phenylbutyrate Controls Neuroinflammatory and Antioxidant Activities and Protects Dopaminergic Neurons in Mouse Models of Parkinson’s Disease
- in-vitro, Nor, glial - in-vivo, NA, NA
*ROS↓, sodium phenylbutyrate (NaPB), an FDA-approved therapy for reducing plasma ammonia and glutamine in urea cycle disorders, can suppress both proinflammatory molecules and reactive oxygen species (ROS) in activated glial cells
*Inflam↑,
*P21↓, Inhibition of both p21ras and p21rac activation by NaPB in microglial cells suggests that NaPB exerts anti-inflammatory and antioxidative effects via inhibition of these small G proteins
*antiOx↑,
*GSH↑, protected nigral reduced glutathione
*NF-kB↓, attenuated nigral activation of NF-κB
*neuroP↑, These results identify novel mode of action of NaPB and suggest that NaPB may be of therapeutic benefit for neurodegenerative disorders.
*HDAC↓, Because NaPB is a known inhibitor of histone deacetylase (HDAC)
*iNOS↓, Similar to the inhibition of iNOS, NaPB dose-dependently inhibited the production of TNF-α and IL-1β protein in activated microglia
*TNF-α↓,
*IL1β↓,
*LDL↓, NaPB reduced the level of cholesterol in serum of mice by about 30%; and this reduction was comparable to that (∼29%) by the so-called cholesterol-lowering drug pravastatin
ROS↓, NaPB strongly inhibited MPP+-induced production of intracellular ROS

4087- VitE,    Vitamin E and Alzheimer's disease: what do we know so far?
- Review, AD, NA
*Risk↑, Diminished circulating concentrations of vitamin E have been demonstrated in individuals with AD. Reduced plasma levels have furthermore been associated with an increased risk of AD
*Half-Life↑, The plasma half-life of α-tocopherol is estimated at 20 hrs, which is considerably longer than that of other isoforms, particularly the tocotrienol congeners
*antiOx↑, potent antioxidant capabilities of vitamin E are well known
*BioAv↑, α-tocopherol retains a superior in vivo role in neuroprotection due to its relatively greater bioavailability and preferential retention by tissues.
*neuroP↑, includes other neuro-protective, anti-inflammatory and cholesterol-reducing properties, in addition to influencing gene expression and potentially ensuing AD pathology.
*Inflam↑,
*LDL↓,
*cognitive↑, vitamin E supplementation was associated with decreased risk of cognitive decline in a cohort of 560 AD patients from the Canadian Study of Health and Aging


Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned ⓘ

NA↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 2,   GSH↓, 1,   lipid-P↑, 1,   MDA↑, 1,   ROS↓, 2,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   LDH↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   p‑Akt↓, 1,   Apoptosis↑, 3,   Bak↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   BIM↑, 1,   Casp↑, 1,   Casp3↑, 3,   Casp9↑, 2,   Cyt‑c↑, 1,   FADD↑, 1,   NOXA↑, 1,   PUMA↑, 1,   survivin↓, 1,   TRAIL↑, 1,  

Transcription & Epigenetics ⓘ

other?, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMTs↓, 1,   P53↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

FOXO3↑, 1,   HDAC↓, 1,   mTOR↓, 1,   p‑PI3K↓, 1,   STAT3↓, 1,   TumCG↓, 2,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 1,   E-cadherin↑, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMP7↓, 1,   MMP9↓, 1,   MMPs↓, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 1,   TumMeta↓, 1,   TumMeta↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↑, 3,   NF-kB↓, 4,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 3,   eff↑, 4,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,   creat↓, 1,   GutMicro↑, 2,   Ki-67↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   Appetite↑, 1,   chemoP↑, 2,   chemoPv↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   Pain↓, 1,   QoL↑, 1,   radioP↑, 2,   RenoP↑, 1,   Sleep↑, 1,  
Total Targets: 82

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

AntiArt↑, 1,   TMAO↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 11,   Catalase↓, 1,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 4,   HO-1↑, 2,   lipid-P↓, 2,   MDA↓, 5,   NRF2↑, 3,   ROS↓, 5,   ROS↑, 2,   SOD↓, 1,   SOD↑, 3,   TAC↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   glucose↓, 1,   LDL↓, 2,   NADPH↑, 1,   PPARγ↓, 1,  

Cell Death ⓘ

Akt↑, 1,   Apoptosis↑, 1,   iNOS↓, 2,   MAPK↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 4,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Cell Cycle & Senescence ⓘ

P21↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   GSK‐3β↑, 1,   HDAC↓, 1,   PI3K↑, 1,  

Migration ⓘ

AntiAg↓, 1,   Ca+2↑, 1,   CLDN1↓, 1,   TJ↓, 1,   ZO-1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

IL10↓, 1,   IL1β↓, 1,   IL4↓, 1,   IL6↓, 2,   Inflam↓, 1,   Inflam↑, 13,   NF-kB↓, 2,   PGE2↓, 1,   TLR2↓, 1,   TLR4↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   ChAT↑, 1,   GABA↑, 1,   MAOA↓, 1,   tau↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,   BACE↓, 1,   NLRP3↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   BioAv⇅, 1,   BioAv↝, 2,   Dose↝, 1,   eff↑, 2,   Half-Life↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   GutMicro↑, 1,   IL6↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 2,   AntiDiabetic↑, 2,   cardioP↑, 2,   cognitive↓, 2,   cognitive↑, 1,   memory↑, 2,   Mood↑, 1,   neuroP↑, 6,   Risk↑, 1,   toxicity↓, 1,   toxicity↑, 1,   toxicity↝, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 2,  
Total Targets: 80

Scientific Paper Hit Count for: Inflam, inflammation
2 Carvacrol
2 Eugenol
1 Astaxanthin
1 Caffeic Acid Phenethyl Ester (CAPE)
1 Thymol-Thymus vulgaris
1 Choline
1 Cinnamon
1 Copper and Cu NanoParticles
1 Curcumin
1 Gallic acid
1 Hydrogen Gas
1 Magnolol
1 Melatonin
1 Chemotherapy
1 Radiotherapy/Radiation
1 Phenylbutyrate
1 Vitamin E
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#:953  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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