ROS Cancer Research Results

ROS, Reactive Oxygen Species: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy 
ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination




Item ROS↑ NRF2 Condition Mechanism Class Remarks 



ROS">Piperlongumine
+++ ↓ [D][T] ROS-dominant






ROS">Shikonin
+++↓/±[D][T]ROS-dominant






ROS">Vitamin K3 (menadione)
+++↓[D]ROS-dominant






ROS">Copper (ionic / nano)
+++↓[Fe][F]ROS-dominant






ROS">Sodium Selenite
+++↓[D]ROS-dominant






ROS">Juglone
+++↓[D]ROS-dominant






ROS">Auranofin
+++↓[D]ROS-dominant






ROS">Photodynamic Therapy (PDT)
+++0[L][O₂]ROS-dominant






ROS">Radiotherapy / Radiation
+++0[O₂]ROS-dominant






ROS">Doxorubicin
+++↓[D]ROS-dominant






ROS">Cisplatin
++↓[D][T]ROS-dominant






ROS">Salinomycin
++↓[D][T]ROS-dominant






ROS">Artemisinin / DHA
++↓[Fe][T]ROS-dominant






ROS">Sulfasalazine
++↓[C][T]ROS-dominant






ROS">FMD / fasting
++↓[M][C][O₂]ROS-dominant






ROS">Vitamin C (pharmacologic)
++↓[Fe][D]ROS-dominant






ROS">Silver nanoparticles
++±[F][D]ROS-dominant






ROS">Gambogic acid
++↓[D][T]ROS-dominant






ROS">Parthenolide
++↓[D][T]ROS-dominant






ROS">Plumbagin
++↓[D]ROS-dominant






ROS">Allicin
++↓[D]ROS-dominant






ROS">Ashwagandha (Withaferin A)
++↓[D][T]ROS-dominant






ROS">Berberine
++↓[D][M]ROS-dominant






ROS">PEITC
++↓[D][C]ROS-dominant






ROS">Methionine restriction
+↓[M][C][T]ROS-secondary






ROS">DCA
+±[M][T]ROS-secondary






ROS">Capsaicin
+±[D][T]ROS-secondary






ROS">Galloflavin
+0[D]ROS-secondary






ROS">Piperine
+±[D][F]ROS-secondary






ROS">Propyl gallate
+↓[D]ROS-secondary






ROS">Scoulerine
+?[D][T]ROS-secondary






ROS">Thymoquinone
±±[D][T]Dual redox






ROS">Emodin
±±[D][T]Dual redox






ROS">Alpha-lipoic acid (ALA)
±↑[D][M]NRF2-dominant






ROS">Curcumin
±↑/↓[D][F]NRF2-dominant






ROS">EGCG
±↑/↓[D][O₂]NRF2-dominant






ROS">Quercetin
±↑/↓[D][Fe]NRF2-dominant






ROS">Resveratrol
±↑[D][M]NRF2-dominant






ROS">Sulforaphane
±↑↑[D]NRF2-dominant






ROS">Lycopene
0↑—Antioxidant






ROS">Rosmarinic acid
0↑—Antioxidant






ROS">Citrate
00—Neutral


AD, Alzheimer's Disease: Click to Expand ⟱
In Alzheimer's disease (AD), cholinergic dysfunction (often with reduced acetylcholine tone and impaired choline metabolism) is linked with cortical dysfunction, memory deficit, abnormal cerebral blood flow, task learning difficulty, sleep-cycle disruption, and neurodevelopmental effects (context-dependent).
CORE HALLMARKS / HIGH-CONFIDENCE AXES:
- tau and Aβ, their accumulation in AD brains is known to be a major hallmark.
  In AD, PP2A↓ activity is decreased (reported), contributing to hyperphosphorylated tau accumulation.
  SIRT-1↓ levels in AD brains are associated with accumulation of Aβ and tau (reported).
- glucose metabolism↓ (brain glucose hypometabolism) occurs in AD long before significant clinical signs in many cohorts/models (reported).
- Neuroinflammation / lipid mediator tone (reported): 5-LOX↑ and PGE2↑ (model-/region-dependent).
- Synaptic vulnerability (reported): PSD95↓ in hippocampus and cortex; restoring PSD95 shows cognitive benefits in models.
- Clearance/transport imbalance (reported): IDE↓, NEP↓, LRP1↓, and AEP↑ protein levels in AD brains (reported).

COMMONLY REPORTED DIRECTIONAL CHANGES (model/region/compartment dependent):
- Monoamines (reported): concentrations of 5-HTP↓, 5-HT(seratonin)↓, and 5-HIAA↓ are lower in Alzheimer's patients (varies by region/study).
- Cholinergic system (clinical target): reduction in ACh↓ production; ChAT↓ activity reduced (synthesizes ACh).
- Four key enzymes frequently targeted in AD symptom/adjunct strategies: AChE, BChE, MAOA, MAOB (objective inhibit).
- Neurotrophic tone (reported): BDNF↓ in key regions.
  - Stress can decrease expression of brain-derived neurotrophic factor (BDNF).
- Kinase/protease stress (reported): CDK5↑ hyperactivation; calpain↑ overactivated by increased intracellular Ca²⁺ → p-tau and aggregation.
- Aβ-linked synaptic regulator (reported): STEP↑ upregulated largely due to Aβ oligomer accumulation.
- α-secretase axis (reported): ADAM10↓ downregulated in AD brains.
- Metabolic cofactors (reported): ALC↓ (ALCAR); Homocarnosine↓ (CSF declines with age); possible low Taurine↓ (age-related + dementia reports).
- Ion/glutamate handling (reported): impaired glutamate clearance + depressed Na+/K+ ATPase → cellular ion imbalance risk.
- Aging reduces NAD⁺↓ (in AD depletion may be more severe).
- Mitochondrial capacity axis (reported): PGC-1↓ decreased in Alzheimer’s brains.
- Innate immune DNA-sensing axis (animal): cGAS–STING↑ elevation observed in AD mice and normalized by NR treatment.
- Vascular/structure (reported): a profound change in BBB permeability; progressive brain shrinkage (atrophy).
- Glycation axis (reported): AGEs↑ and RAGE↑ expression.

HOMOCYSTEINE / B-VITAMIN AXIS:
- Raised plasma total homocysteine (tHcy)↑ associated with cognitive impairment, AD, or vascular dementia (epidemiology).
  - Homocysteine can build up if vitamin B6, B12, or folate levels are low.
  - Homocysteine and B-vitamin in Cognitive Impairment (VITACOG) study.
  - Vit B6 might be an important B vitamin (often discussed along with B12 and folate).
- Thiamine↓ deficiency produces a cholinergic deficit (well-aligned with AD features).
- Decreased thiamine (B1) in AD may exacerbate Aβ deposition, tau hyperphosphorylation, and oxidative stress (reported).

MICRONUTRIENTS / CAROTENOIDS (reported; compartment-dependent):
- vitamin A↓ and β-carotene↓ lower in some AD cohorts; excess retinol may contribute to osteoporosis risk.
- Diminished circulating vitamin E↓ reported in AD.
- Vitamin B5↓ in multiple brain regions (reported).
- Trace elements: patients with AD reported lower serum Se, Cu, and Zn↓ (serum findings vary by study).
- Brain metals: some studies report higher brain copper↑ and iron↑ in specific regions/structures; compartment and region matter.
  Rosmarinic acid reported to reduce copper-induced neurotoxicity in vitro/in vivo and may interfere with amyloid–copper interactions (preclinical).
- SAMe↓ concentrations in CSF reported in AD.
- MPOD often reduced in AD patients.
- AD brains reported lower levels of lutein↓, zeaxanthin↓, anhydrolutein↓, (VitA)retinol↓, lycopene↓, alpha-tocopherol↓.

RISK CONTEXT:
- Apolipoprotein E4 (ApoE4) genotype is the strongest known genetic risk factor for late-onset AD.
  - One copy of ApoE4: ~3–4× increased risk (range varies by cohort).
  - Two copies: ~8–12× increased risk (range varies).
  - VitK lower in circulating blood of APOE4 carriers (reported).
- Type 2 diabetes, traumatic brain injury, stroke, diet, and above all, aging is the number ONE risk factor.

Treatments / Strategy Targets (high-level):
- Early intervention tends to have a greater positive effect than interventions during middle or late stages.
- BOLD fMRI imaging can be used to observe brain activity via blood oxygen/flow changes.
- Reduce ROS and inflammation in the brain (context-dependent; avoid over-suppressing adaptive signaling).
- Inhibiting acetylcholinesterase (AChE) (which breaks down ACh), e.g., donepezil, rivastigmine.
- Natural AChE inhibitors include: Berberine, Luteolin, Crocetin(saffron), Querctin, TQ
- Natural AChE inhibitors in database (check BBB pass potential).
- MAOB inhibitors, APP inhibitors, PGE2 inhibitors, NLRP3 inhibitors, BACE inhibitors
- BDNF activators, PSD95 activator
- STEP, ADAM10
- Diets with an adequate ratio (5:1) of omega-6:3 (Mediterranean diet).
- Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects (general nutrition framing).
- Antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin).
- Fiber may promote gut microbiome diversity influencing brain health.
- Supplementing with NAD⁺ precursors (NR or NMN) improves cognition and reduces amyloid/tau pathologies in AD mice (animal evidence).
- "It is advisable to consume diets with an adequate ratio (5:1) of omega-6:3 fatty acids (Mediterranean diet) ... antioxidants ... role in oxidative stress ... cognition." Nutrition Strategies
- Reduction of cognitive decline may be achieved by following a healthy dietary pattern limiting added sugars while maximizing fish, fruits, vegetables, nuts, seeds.

SeNPs may also be useful as a Drug Delivery System.


Related Pathways to research in this database (products that modulate them):
- neuroprotective, cognitive, memory
- Aβ aggregation, Tau↓, AChE↓, ACh↑, ChAT↑, acetyl-CoA↑, BDNF↑, BACE↓, NLRP3↓, PSD95↑, PGE2↓, homoC↓
- Increasing AntiOxidants: Catalase↑, GSH↑, SOD↑, HO-1↑, to decrease ROS↓
- Lower Inflammation: TNF-α↓, IL1β↓, IL6↓

Natural Products that may benefit AD.
-Some key pathways are highlighted in RED in the following links
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Acetyl-L-carnitine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">ALA, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Apigenin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Anthocyanins Blueberrys, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Aromatherapy, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Artemisinin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ashwagandha,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">β-carotene(vitamin A), ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Bacopa monnieri, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Baicalein, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Baicalin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Berberine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Betulinic acid, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Boron, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Boswellia (frankincense),
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Caffeic acid, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Caffeine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Capsaicin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Carnosine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Carnosic acid, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Chlorogenic acid, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Choline, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Chrysin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Cinnamon, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">CoQ10, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Crocetin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Curcumin,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">dietMed, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">dietMet, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">dietSTF, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">EGCG, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ellagic acid, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Exercise, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ferulic Acid, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Fisetin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Flav, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">FLS, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Folic Acid (5-MTHF, L-methylfolate)-reduce homocysteine,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Galantamine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ginger, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ginkgo biloba, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ginseng,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Honokiol, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Huperzine A, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">hydrogen gas, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Lecithin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Lutein, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Luteolin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Lycopene,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">M-Blu, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Moringa oleifera, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Mushroom Lion’s Mane, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">MSM, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">MCToil, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">NAD, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Naringenin,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">PEMF, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Piperine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Phenylbutyrate, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Phosphatidylserine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Piperlongumine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Potassium, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">probiotics, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Propolis, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Pterostilbene,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Quercetin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Resveratrol, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Rivastigmine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Rosmaric Acid(reduce copper-induced neurotoxicity), ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Rutin,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Safflower yellow, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Sage, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">SAMe, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">selenium, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Serotonin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Shankhpushpi, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Shikonin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Shilajit/Fulvic Acid, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">silicon(reduce Alum bioavialability), ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Silymarin (Milk Thistle) silibinin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Sulforaphane,
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Taurine, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">TQ, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Ursolic Acid
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B1, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B2, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B3, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B5, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B6, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin B12, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin E, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin D, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Vitamin K2
ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Zeaxanthin, ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">zinc,

ROS&w19=NRF2&w20=Catalase &w21=GSH&w22=SOD&w23=HO-1&w24=PGE2&w25=Inflam&w26=NF-kB&w27= IL1β&w28=TNF-α">Aluminium has a negative impact on cognition but silicon can decrease Alumunium bioavailability, and Vitamin K2 may provide some protection. Example So does RMF

Brain Energy Systems Matrix (AD)

Tier 1–2 as “core metabolic cofactors / redox pools”
Tier 4 as “alternative fuels / bypass strategies”
Tier 5–6 as “capacity + delivery constraints” (often explains why supplements don’t translate)
Tier Rank Node / Lever What it Supports (Bioenergetic Role) Key Enzymes / Targets AD-Relevant Mechanism TSF Evidence Common Constraints / Gotchas
11 Thiamine (B1) / TPP Glucose → acetyl-CoA entry + TCA throughput + NADPH support PDH, α-KGDH, Transketolase (PPP) Addresses cerebral glucose hypometabolism; improves mitochondrial flux; PPP→NADPH supports redox R, G Mechanistic + small clinical Benefit strongest if low status; standard thiamine vs lipophilic derivatives differ
12 Benfotiamine Higher-bioavailability B1 strategy Transketolase ↑; glycation axis ↓ AGE/RAGE burden reduction + metabolic support (model/trial dependent) G Small clinical + mechanistic Not a “rapid” effect; mostly longer-term metabolic/toxicity load reduction
13 Riboflavin (B2) / FAD, FMN ETC redox enzymes + mitochondrial dehydrogenases Complex I/II flavoproteins; many oxidoreductases Supports electron handling; can be limiting in mitochondrial enzyme insufficiency R, G Mechanistic Direct AD cognitive trial support limited; “helps” mostly when deficient or enzyme-limited
14 Niacin forms (B3) → NAD pool NAD+/NADH redox + signaling + repair NAD salvage; sirtuins; PARP substrate NAD decline is an aging/inflammation theme; supports mitochondrial redox capacity R, G Emerging human + mechanistic Different forms behave differently; NAD raising ≠ guaranteed clinical cognition benefit
15 Pantothenic acid (B5) → CoA Acetyl-CoA formation; lipid metabolism; TCA entry CoA biosynthesis; acetylation capacity Foundational for fuel oxidation and acetylation balance G Mechanistic Often overlooked; deficiency uncommon but suboptimal intake can matter in frailty
16 Magnesium ATP handling (Mg-ATP) + enzyme kinetics ATP-dependent enzymes; synaptic function Supports neuronal energy usage + plasticity; deficiency can worsen excitotoxic vulnerability R, G Supportive human + mechanistic Form/absorption variability; renal constraints for supplementation in some patients
21 NAD+ precursors (NR/NMN/NA/NAM) Restores NAD+ availability for redox + signaling NAMPT salvage; sirtuins; PARPs; CD38 Supports mitochondrial function; may improve resilience under oxidative/repair load R, G Animal > human (emerging) NAD “sinks” (CD38/PARP) can dominate; response varies by inflammation/age
22 Alpha-lipoic acid (ALA) Mitochondrial redox cofactor + antioxidant recycling PDH/α-KGDH cofactor; GSH recycling support Improves redox tone and mitochondrial efficiency (signals strongest in metabolic/oxidative phenotypes) R, G Small AD trials + mechanistic “Antioxidant” framing can be misleading—main value is mitochondrial/redox coupling support
23 Glutathione system support Detox + peroxide handling GSH, GPx, GR, NADPH supply (PPP) Reduces oxidative damage load that impairs mitochondria/synapses R, G Mechanistic GSH depends on substrates + NADPH; pushing one component may not fix system
24 Selenium (GPx capacity) Peroxide detox via selenoenzymes Glutathione peroxidases Supports antioxidant enzyme capacity (context-dependent) G Mixed human Narrower safety margin; avoid “more is better” mindset
31 CoQ10 (ubiquinone) ETC electron carrier (I/II→III) + membrane redox Complex I/II→III transfer Supports OXPHOS efficiency; may reduce electron leak under some conditions R, G Limited AD-specific Bioavailability/formulation matters; AD cognition data not robust
32 Cardiolipin / mitochondrial membranes (support axis) ETC supercomplex stability; cristae integrity Inner mitochondrial membrane architecture Membrane integrity affects ETC efficiency and ROS leak G Mechanistic Hard to “target” nutritionally in a clean way; effects indirect
33 Iron / copper homeostasis (burden control) Prevents metal-catalyzed oxidative damage Fenton chemistry burden; metal transport/storage Metal dyshomeostasis can amplify ROS and mitochondrial injury R, G Mechanistic + mixed human “Chelation” is not casually safe; needs careful framing and evidence
41 Ketone utilization (BHB/acetoacetate axis) Alternative brain fuel bypassing glucose bottlenecks MCT1/2 transport; ketolysis enzymes Addresses brain glucose hypometabolism by providing alternate substrate R, G Moderate (human MCI/AD signals exist) GI tolerance and adherence; response varies by genotype/metabolic status
42 Creatine / phosphocreatine shuttle ATP buffering and rapid energy stabilization Creatine kinase system May stabilize energy during stress; supports muscle/functional reserve that impacts cognition indirectly G Limited AD CNS benefit uncertain; stronger for muscle/functional outcomes
43 Acetyl-L-carnitine (ALCAR) Fatty acid oxidation support + acetyl group handling Carnitine shuttle; acetyl-CoA support May support mitochondrial energy and neuronal function (mixed clinical results) R, G Mixed human Benefits heterogeneous; not a universal cognitive improver
44 Medium-chain triglycerides (MCT oil → ketones) Rapid ketone support strategy Hepatic ketogenesis; brain ketone uptake Practical ketone-raising approach for some phenotypes R, G Moderate human GI effects; calorie load; titration matters
51 AMPK → PGC-1α biogenesis axis Mitochondrial number/quality regulation AMPK, PGC-1α, SIRT1 Supports long-term mitochondrial capacity and stress resistance G Mechanistic Most effects are slow; many “activators” are indirect and context-dependent
52 Mitophagy / autophagy quality control Removes damaged mitochondria PINK1/Parkin axis; autophagy machinery Damaged mitochondria drive ROS and energy failure; quality control is protective in theory G Mechanistic Autophagy modulation is double-edged; oversimplified “more autophagy = good” is risky
53 Exercise signaling (the “master cofactor”) Improves vascular + mitochondrial + neurotrophic tone BDNF; insulin sensitivity; AMPK/PGC-1α Most evidence-backed multi-pathway energy intervention for aging brain R, G Strong (human) Adherence/ability constraints; must be individualized
61 Cerebral perfusion / vascular health Fuel + oxygen delivery and waste clearance support Neurovascular unit; endothelial function Vascular dysfunction worsens hypometabolism and inflammation R, G Strong (human) Often upstream of “supplement” efficacy; if delivery is poor, cofactors underperform
62 Sleep / glymphatic clearance Waste clearance & metabolic recovery Glymphatic system; circadian regulation Supports clearance of metabolic byproducts; indirectly supports energy balance G Strong (human) Often neglected; impacts cognition and inflammation strongly
63 Oxygen utilization context (respiratory capacity) Oxidative metabolism support OXPHOS dependence If oxygen delivery/usage is limited, pushing mitochondrial cofactors won’t fully translate R, G Supportive More about system constraints than a “node to supplement”

TSF (Time-Scale Flag): P = 0–30 min, R = 30 min–3 hr, G = >3 hr (adaptation/phenotype). Evidence: "Strong (human)" = consistent clinical/epidemiologic support; "Moderate" = mixed but plausible human signals; "Emerging" = early-stage human; "Mechanistic" = preclinical/biochemical rationale.



Scientific Papers found: Click to Expand⟱
2660- AL,    Allicin: A review of its important pharmacological activities
- Review, AD, NA - Review, Var, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, AntiCan↑, *antiOx↑, *cardioP↑, *hepatoP↑, *BBB↑, *Half-Life↝, *H2S↑, *BP↓, *neuroP↑, *cognitive↑, *neuroP↑, *ROS↓, *GutMicro↑, *LDH↓, *ROS↓, *lipid-P↓, *antiOx↑, *other↑, *PI3K↓, *Akt↓, *NF-kB↓, *NO↓, *iNOS↓, *PGE2↓, *COX2↓, *IL6↓, *TNF-α↓, *MPO↓, *eff↑, *NRF2↑, *Keap1↓, *TBARS↓, *creat↓, *LDH↓, *AST↓, *ALAT↓, *MDA↓, *SOD↑, *GSH↑, *GSTs↑, *memory↑, chemoP↑, IL8↓, Cyt‑c↑, Casp3↑, Casp8↑, Casp9↑, Casp12↑, p38↑, Fas↑, P53↑, P21↑, CHK1↓, CycB/CCNB1↓, GSH↓, ROS↑, TumCCA↑, Hif1a↓, Bcl-2↓, VEGF↓, TumCMig↓, STAT3↓, VEGFR2↓, p‑FAK↓,
3438- ALA,    The Potent Antioxidant Alpha Lipoic Acid
- Review, NA, NA - Review, AD, NA
*antiOx↑, *cardioP↑, *cognitive↑, *AntiAge↑, *Inflam↓, *AntiCan↑, *neuroP↑, *IronCh↑, *ROS↑, *Weight↓, *Ach↑, *ROS↓, *GSH↑, *lipid-P↓, *memory↑, *NRF2↑, *ChAT↑, *GlucoseCon↑, *Acetyl-CoA↑,
3443- ALA,    Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention
- Review, Var, NA - Review, AD, NA
*antiOx↑, *ROS↓, *IronCh↑, *cognitive↑, *cardioP↓, AntiCan↑, *neuroP↑, *Inflam↓, *BioAv↓, *AntiAge↑, *Half-Life↓, *BioAv↝, other↝, EGFR↓, Akt↓, ROS↓, TumCCA↑, p27↑, PDH↑, Glycolysis↓, ROS↑, *eff↑, *memory↑, *motorD↑, *GutMicro↑,
297- ALA,    Insights on the Use of α-Lipoic Acid for Therapeutic Purposes
- Review, BC, SkBr3 - Review, neuroblastoma, SK-N-SH - Review, AD, NA
PDH↑, TumCG↓, ROS↑, AMPK↑, EGR4↓, Half-Life↓, BioAv↝, *GSH↑, *IronCh↑, *ROS↓, *antiOx↑, *neuroP↑, *Ach↑, *lipid-P↓, *IL1β↓, *IL6↓, TumCP↓, FDG↓, Apoptosis↑, AMPK↑, mTOR↓, EGFR↓, TumCI↓, TumCMig↓, *memory↑, *BioAv↑, *BioAv↝, *other↓, *other↝, *Half-Life↓, *BioAv↑, *ChAT↑, *GlucoseCon↑,
2626- Ba,    Molecular targets and therapeutic potential of baicalein: a review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
AntiCan↓, *neuroP↑, *cardioP↑, *hepatoP↑, *RenoP↑, TumCCA↑, CDK4↓, cycD1/CCND1↓, cycE/CCNE↑, BAX↑, Bcl-2↓, VEGF↓, Hif1a↓, cMyc↓, NF-kB↓, ROS↑, BNIP3↑, *neuroP↑, *cognitive↑, *NO↓, *iNOS↓, *COX2↓, *PGE2↓, *NRF2↑, *p‑AMPK↑, *Ferroptosis↓, *lipid-P↓, *ALAT↓, *AST↓, *Fas↓, *BAX↓, *Apoptosis↓,
5633- BCA,    Mechanisms Behind the Pharmacological Application of Biochanin-A: A review
- Review, Var, NA - Review, AD, NA
*AntiDiabetic↑, *neuroP↑, *toxicity↓, *CYP19↓, p‑Akt↓, mTOR↓, TumCCA↑, P21↑, Casp3↑, Bcl-2↑, Apoptosis↑, E-cadherin↓, TumMeta↓, eff↑, GSK‐3β↓, β-catenin/ZEB1↓, RadioS↑, ROS↑, Casp1↑, MMP2↓, MMP9↓, EGFR↓, ChemoSen↑, PI3K↓, MMPs↓, Hif1a↓, VEGF↓, *ROS↓, *Obesity↓, *cardioP↑, *NRF2↑, *NF-kB↓, *Inflam↓, *lipid-P↓, *hepatoP↑, *AST↓, *ALP↓, *Bacteria↓, *neuroP↑, *SOD↑, *GPx↑, *AChE↓, *BACE↓, *memory↑, *BioAv↓,
2775- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
ROS↑, ER Stress↑, TumCG↓, Apoptosis↑, Inflam↓, ChemoSen↑, Casp↑, ERK↓, cl‑PARP↑, AR↓, cycD1/CCND1↓, VEGFR2↓, CXCR4↓, radioP↑, NF-kB↓, VEGF↓, P21↑, Wnt↓, β-catenin/ZEB1↓, Cyt‑c↑, MMP2↓, MMP1↓, MMP9↓, PI3K↓, MAPK↓, JNK↑, *5LO↓, *NRF2↑, *HO-1↑, *MDA↓, *SOD↑, *hepatoP↑, *ALAT↓, *AST↓, *LDH↑, *CRP↓, *COX2↓, *GSH↑, *ROS↓, *Imm↑, *Dose↝, *eff↑, *neuroP↑, *cognitive↑, *IL6↓, *TNF-α↓,
5858- CAP,    Capsaicin as a Microbiome Modulator: Metabolic Interactions and Implications for Host Health
- Review, Nor, NA - Review, AD, NA
*BBB↓, *GutMicro↑, Obesity↓, *Inflam↓, *AntiCan↑, *TRPV1↑, *Ca+2↑, *antiOx↑, *cardioP↑, *BioAv↓, *Half-Life↓, *BioAv↝, *BioAv↑, *neuroP↑, Apoptosis↑, p38↑, ROS↑, MMP↓, MPT↑, Cyt‑c↑, Casp↑, TRIB3↑, NADH↓, SIRT1↓, TumCG↓, TumCMig↓, TOP1↓, TOP2↓, β-catenin/ZEB1↓, *ROS↓, *Aβ↓,
5854- CAP,    Pharmacological activity of capsaicin: Mechanisms and controversies (Review)
- Review, Var, NA - Review, AD, NA
Obesity↓, Half-Life↓, antiOx↑, TRPV1↑, STAT3↓, Ca+2↑, ROS↑, MMP↓, *neuroP↑, *tau↓, *Inflam↓, *ROS?,
5943- Cela,    Celastrol: A Spectrum of Treatment Opportunities in Chronic Diseases
- Review, Arthritis, NA - Review, IBD, NA - Review, AD, NA - Review, Park, NA
*other↝, *other↝, *CRP↓, *eff↝, *other↑, *CXCR4↓, *IL1β↓, *IL6↓, *IL17↓, *IL18↓, *TNF-α↓, *MMP9↓, *PGE2↓, *COX1↓, *COX2↓, *PI3K↓, *Akt↓, *other↑, TumCCA↑, Apoptosis↑, ROS↑, JNK↑, TumAuto↑, Hif1a↓, BNIP3↝, HSP90↓, Fas↑, FasL↑, ETC↓, VEGF↓, angioG↓, RadioS↑, *neuroP↑, *HSP70/HSPA5↑, *ROS↓, *MMP↑, *Cyt‑c↓, *Casp3↓, *Casp9↓, *MAPK↓, *Dose⇅, *HSPs↑, BioAv↓, Dose↝,
6002- CGA,    Chlorogenic Acid: A Systematic Review on the Biological Functions, Mechanistic Actions, and Therapeutic Potentials
- Review, Var, NA - Review, Diabetic, NA - Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, *Inflam↓, *antiOx↑, *cardioP↑, *NRF2↑, *AMPK↑, *SOD↑, *Catalase↑, *GSH↑, *GPx↑, *ROS↓, *TNF-α↓, *IL6↓, *NF-kB↓, *COX2↓, *glucose↓, *TRPC1↓, *Ca+2↓, *HO-1↑, *NF-kB↓, *PPARα↝, *Hif1a↓, *JNK↓, *BP↓, *AntiDiabetic↑, *hepatoP↑, *TLR4↓, *NRF2↑, *Casp↓, *neuroP↑, *Aβ↓, *LDH↓, *MDA↓, *memory↑, *AChE↓, *eff↑, EMT↝, N-cadherin↓, E-cadherin↑, TumCCA↑, ROS↑, p‑P53↑, HO-1↑, NRF2↑, ChemoSen↑, mtDam↑, Casp3↑, Casp9↑, PARP↑, Bax:Bcl2↑, TumCG↓, cycD1/CCND1↓, cMyc↓, CDK2↓, mitResp↓, Glycolysis↓, Hif1a↓, PCNA↓, p‑GSK‐3β↓, VEGF↓, PI3K↓, Akt↓, mTOR↓, OS↑,
6108- Chol,    Trimethylamine-N-Oxide (TMAO) as a Rising-Star Metabolite: Implications for Human Health
- Review, Nor, NA - Review, AD, NA
*TMAO↑, *ROS↑, *NADPH↑, *Ca+2↑, *AntiAg↓, *cognitive↓, *TJ↓, *CLDN1↓, *ZO-1↓, *Inflam↑, *NLRP3↑, *ER Stress↑, *cognitive↓, *Dose↝, *eff↑, *other↝, *other↝, *other↝,
2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, *SOD↑, p16↑, JAK2↓, STAT3↓, CXCL12↓, IL6↓, MMP2↓, MMP9↓, TGF-β↓, α-SMA↓, LAMs↓, DNAdam↑, *memory↑, *cognitive↑, *Inflam↓, *antiOx↑, *NO↑, *MDA↓, *ROS↓, DNMT1↓, ROS↑, Casp3↑, Apoptosis↑, miR-21↓, LC3II↓, ChemoSen↑, NF-kB↓, CSCs↓, Nanog↓, OCT4↓, SOX2↓, eff↑, Sp1/3/4↓, miR-27a-3p↓, ZBTB10↑, SOX9?, ChemoSen↑, VEGF↓, XIAP↓, Bcl-2↓, cycD1/CCND1↓, BioAv↑, Hif1a↓, EMT↓, BioAv↓, PTEN↑, VEGF↓, Akt↑, EZH2↓, NOTCH1↓, TP53↑, NQO1↑, HO-1↑,
3205- EGCG,    The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas
- Review, Var, NA - Review, AD, NA
Beclin-1↑, ROS↑, Apoptosis↑, ER Stress↑, *Inflam↓, *cardioP↑, *antiOx↑, *LDL↓, *NF-kB↓, *MPO↓, *glucose↓, *ROS↓, ATG5↑, LC3B↑, MMP↑, lactateProd↓, VEGF↓, Zeb1↑, Wnt↑, IGF-1R↑, Fas↑, Bak↑, BAD↑, TP53↓, Myc↓, Casp8↓, LC3II↑, NOTCH3↓, eff↑, p‑Akt↓, PARP↑, *Cyt‑c↓, *BAX↓, *memory↑, *neuroP↑, *Ca+2?, GRP78/BiP↑, CHOP↑, ATF4↑, Casp3↑, Casp8↑, UPR↑,
5113- JG,    Juglone in Oxidative Stress and Cell Signaling
- Review, Var, NA - Review, AD, NA
ROS↑, Pin1↓, antiOx⇅, *ROS↓, SMAD2↓, GSH↓, lipid-P↑, TumCCA↓, BAX↑, Bcl-2↓, Casp3↑, Casp9↑, Ca+2↑, Cyt‑c↑, AntiFungal↑, Bacteria↓, Akt↓,
2916- LT,    Antioxidative and Anticancer Potential of Luteolin: A Comprehensive Approach Against Wide Range of Human Malignancies
- Review, Var, NA - Review, AD, NA - Review, Park, NA
proCasp9↓, CDC2↓, CycB/CCNB1↓, Casp9↑, Casp3↑, Cyt‑c↑, cycA1/CCNA1↑, CDK2↓, APAF1↑, TumCCA↑, P53↑, BAX↑, VEGF↓, Bcl-2↓, Apoptosis↑, p‑Akt↓, p‑EGFR↓, p‑ERK↓, p‑STAT3↓, cardioP↑, Catalase↓, SOD↓, *BioAv↓, *antiOx↑, *ROS↓, *NO↓, *GSTs↑, *GSR↑, *SOD↑, *Catalase↑, *lipid-P↓, PI3K↓, Akt↓, CDK2↓, BNIP3↑, hTERT/TERT↓, DR5↑, Beclin-1↑, TNF-α↓, NF-kB↓, IL1↓, IL6↓, EMT↓, FAK↓, E-cadherin↑, MDM2↓, NOTCH↓, MAPK↑, Vim↓, N-cadherin↓, Snail↓, MMP2↓, Twist↓, MMP9↓, ROS↑, MMP↓, *AChE↓, *MMP↑, *Aβ↓, *neuroP↑, Trx1↑, ROS↓, *NRF2↑, NRF2↓, *BBB↑, ChemoSen↑, GutMicro↑,
3900- MCT,    Coconut (Cocos nucifera) Ethanolic Leaf Extract Reduces Amyloid-β (1-42) Aggregation and Paralysis Prevalence in Transgenic Caenorhabditis elegans Independently of Free Radical Scavenging and Acetylcholinesterase Inhibition
- in-vitro, AD, NA
*ROS↑, *AChE↓, *Aβ↓,
1778- MEL,    Melatonin: a well-documented antioxidant with conditional pro-oxidant actions
- Review, Var, NA - Review, AD, NA
*ROS↓, *antiOx↓, ROS↑, selectivity↑, Dose↑, *mitResp↑, *ATP↑, *ROS↓, eff↑, ROS↑, Dose↑, *toxicity∅, ROS↑, eff↓, ROS↝, Dose↑, other↑,
5795- MET,    Metformin: A Review of Potential Mechanism and Therapeutic Utility Beyond Diabetes
- Review, AD, NA - Review, Park, NA - Review, Diabetic, NA
*AntiDiabetic↑, *AMPK↑, *glyC↓, *ROS↓, *cardioP↑, *neuroP↑, *Half-Life↝, *toxicity↝, *BioAv↑, *glucose↓, *AGEs↓, AntiCan↑, Risk↓, TumCP↓, Apoptosis↑, TumCCA↑, cycD1/CCND1↓, pRB↓, p27↓, mTOR↓, Casp↑, ROS↑, MMP↓, ChemoSen↑, *hepatoP↑, *CRM↑, *Insulin↓,
3924- PTS,    Effect of resveratrol and pterostilbene on aging and longevity
- Review, AD, NA - Review, Stroke, NA
*antiOx↓, *ROS↑, *SOD↑, *GSH↑, *NRF2↑, *MDA↓, *HNE↓, *Inflam↓, *MAPK↓, *IL6↓, *TNF-α↓, *HO-1↑, *cardioP↑, *neuroP↑, *CRM↑, *NLRP3↓,
3374- QC,    Therapeutic effects of quercetin in oral cancer therapy: a systematic review of preclinical evidence focused on oxidative damage, apoptosis and anti-metastasis
- Review, Oral, NA - Review, AD, NA
α-SMA↓, α-SMA↑, TumCP↓, tumCV↓, TumVol↓, TumCI↓, TumMeta↓, TumCMig↓, ROS↑, Apoptosis↑, BioAv↓, *neuroP↑, *antiOx↑, *Inflam↓, *Aβ↓, *cardioP↑, MMP↓, Cyt‑c↑, MMP2↓, MMP9↓, EMT↓, MMPs↓, Twist↓, Slug↓, Ca+2↑, AIF↑, Endon↑, P-gp↓, LDH↑, HK2↓, PKA↓, Glycolysis↓, GlucoseCon↓, lactateProd↓, GRP78/BiP↑, Casp12↑, CHOP↑,
2687- RES,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, NA, NA - Review, AD, NA
NF-kB↓, P450↓, COX2↓, Hif1a↓, VEGF↓, *SIRT1↑, SIRT1↓, SIRT2↓, ChemoSen⇅, cardioP↑, *memory↑, *angioG↑, *neuroP↑, STAT3↓, CSCs↓, RadioS↑, Nestin↓, Nanog↓, TP53↑, P21↑, CXCR4↓, *BioAv↓, EMT↓, Vim↓, Slug↓, E-cadherin↑, AMPK↑, MDR1↓, DNAdam↑, TOP2↓, PTEN↑, Akt↓, Wnt↓, β-catenin/ZEB1↓, cMyc↓, MMP7↓, MALAT1↓, TCF↓, ALDH↓, CD44↓, Shh↓, IL6↓, VEGF↓, eff↑, HK2↓, ROS↑, MMP↓,
4608- SeNPs,    Selenium Nanoparticles for Biomedical Applications: From Development and Characterization to Therapeutics
- Review, Var, NA - NA, AD, NA
*toxicity↝, *toxicity↓, *other↝, ROS↑, *Dose↝, *selenoP↑, AntiCan↑, AntiTum↑, *Bacteria↓, *radioP↑, *BioAv↑, *Inflam↓, *Imm↑, ChemoSen↑, *AntiAg↑, selectivity↑, eff↑, other↝, *eff↑, *Aβ↓, *eff↑,
4891- Sper,    Spermidine as a promising anticancer agent: Recent advances and newer insights on its molecular mechanisms
- Review, Var, NA - Review, AD, NA
TumCCA↑, TumCP↓, TumCG↓, *Inflam↓, *antiOx↑, *neuroP↑, *cognitive↑, *Aβ↓, *mitResp↑, AntiCan↑, TumCD↑, TumAuto↑, *AntiAge↑, LC3B-II↑, ATG5↑, Beclin-1↑, mt-ROS↑, H2O2↑, Apoptosis↑, *ROS↑, ChemoSen↑, MMP↓, Cyt‑c↑,
5904- TV,    Pharmacological Properties and Molecular Mechanisms of Thymol: Prospects for Its Therapeutic Potential and Pharmaceutical Development
- Review, Var, NA - Review, Stroke, NA - Review, Diabetic, NA - Review, Obesity, NA - Review, AD, NA - Review, Arthritis, NA
*antiOx↑, *ROS↓, *Inflam↓, *Bacteria↓, AntiTum↑, IronCh↑, *HDL↑, *LDL↓, *BioAv↝, *Half-Life↝, *BioAv↑, *SOD↑, *GPx↑, *GSTs↑, *eff↑, radioP↑, *MDA↓, *other↑, *COX1↓, *COX2↓, *AntiAg↑, *RNS↓, *NO↓, *H2O2↓, *NOS2↓, *NADH↓, *Imm↑, Apoptosis↑, TumCP↓, angioG↓, TumCMig↓, Ca+2↑, TumCCA↑, DNAdam↑, BAX↑, Casp9↑, Casp8↑, Casp3↑, cl‑PARP↑, AIF↑, i-ROS↑, MMP↓, Cyt‑c↑, APAF1↑, Ca+2↑, MMP9↓, MMP2↓, PKCδ↓, ERK↓, H2O2↑, BAX↑, Bcl-2↓, DNAdam↑, lipid-P↑, ChemoSen↑, chemoP↑, *cardioP↑, *SOD↑, *Catalase↑, *GPx↑, *GSH↑, *BP↓, *AntiDiabetic↑, *Obesity↓, RenoP↑, *GastroP↑, hepatoP↑, *AChE↓, *cognitive↑, *BChE↓, *other↓, *BioAv↑,

Showing Research Papers: 1 to 25 of 25

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 25

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   antiOx⇅, 1,   Catalase↓, 1,   GSH↓, 2,   H2O2↑, 2,   HO-1↑, 2,   lipid-P↑, 2,   NADH↓, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 1,   ROS↓, 2,   ROS↑, 21,   ROS↝, 1,   i-ROS↑, 1,   mt-ROS↑, 1,   SOD↓, 1,   Trx1↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 2,   CDC2↓, 1,   ETC↓, 1,   mitResp↓, 1,   MMP↓, 8,   MMP↑, 1,   MPT↑, 1,   mtDam↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 3,   cMyc↓, 3,   FDG↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   HK2↓, 2,   lactateProd↓, 2,   LDH↑, 1,   PDH↑, 2,   SIRT1↓, 2,   SIRT2↓, 1,  

Cell Death ⓘ

Akt↓, 5,   Akt↑, 1,   p‑Akt↓, 3,   APAF1↑, 2,   Apoptosis↑, 12,   BAD↑, 1,   Bak↑, 1,   BAX↑, 5,   Bax:Bcl2↑, 1,   Bcl-2↓, 6,   Bcl-2↑, 1,   Casp↑, 3,   Casp1↑, 1,   Casp12↑, 2,   Casp3↑, 8,   Casp8↓, 1,   Casp8↑, 3,   Casp9↑, 5,   proCasp9↓, 1,   Cyt‑c↑, 8,   DR5↑, 1,   Endon↑, 1,   Fas↑, 3,   FasL↑, 1,   hTERT/TERT↓, 1,   JNK↑, 2,   MAPK↓, 1,   MAPK↑, 1,   MDM2↓, 1,   Myc↓, 1,   p27↓, 1,   p27↑, 1,   p38↑, 2,   TRPV1↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

SOX9?, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,   miR-21↓, 1,   miR-27a-3p↓, 1,   other↑, 1,   other↝, 2,   pRB↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   ER Stress↑, 2,   GRP78/BiP↑, 2,   HSP90↓, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 2,   Beclin-1↑, 3,   BNIP3↑, 2,   BNIP3↝, 1,   LC3B↑, 1,   LC3B-II↑, 1,   LC3II↓, 1,   LC3II↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↑, 4,   DNMT1↓, 1,   p16↑, 1,   P53↑, 2,   p‑P53↑, 1,   PARP↑, 2,   cl‑PARP↑, 2,   PCNA↓, 1,   TP53↓, 1,   TP53↑, 2,  

Cell Cycle & Senescence ⓘ

CDK2↓, 3,   CDK4↓, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 5,   cycE/CCNE↑, 1,   P21↑, 4,   TumCCA↓, 1,   TumCCA↑, 10,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 1,   CD44↓, 1,   CSCs↓, 2,   EMT↓, 4,   EMT↝, 1,   ERK↓, 2,   p‑ERK↓, 1,   GSK‐3β↓, 1,   p‑GSK‐3β↓, 1,   IGF-1R↑, 1,   mTOR↓, 4,   Nanog↓, 2,   Nestin↓, 1,   NOTCH↓, 1,   NOTCH1↓, 1,   NOTCH3↓, 1,   OCT4↓, 1,   PI3K↓, 4,   PTEN↑, 2,   Shh↓, 1,   SOX2↓, 1,   STAT3↓, 4,   p‑STAT3↓, 1,   TCF↓, 1,   TOP1↓, 1,   TOP2↓, 2,   TumCG↓, 5,   Wnt↓, 2,   Wnt↑, 1,  

Migration ⓘ

Ca+2↑, 5,   CXCL12↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 3,   FAK↓, 1,   p‑FAK↓, 1,   LAMs↓, 1,   MALAT1↓, 1,   MMP1↓, 1,   MMP2↓, 6,   MMP7↓, 1,   MMP9↓, 6,   MMPs↓, 2,   N-cadherin↓, 2,   PKA↓, 1,   PKCδ↓, 1,   Slug↓, 2,   SMAD2↓, 1,   Snail↓, 1,   TGF-β↓, 1,   TRIB3↑, 1,   TumCI↓, 2,   TumCMig↓, 5,   TumCP↓, 5,   TumMeta↓, 2,   Twist↓, 2,   Vim↓, 2,   Zeb1↑, 1,   α-SMA↓, 2,   α-SMA↑, 1,   β-catenin/ZEB1↓, 4,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 1,   EGFR↓, 3,   p‑EGFR↓, 1,   EGR4↓, 1,   Hif1a↓, 7,   VEGF↓, 12,   VEGFR2↓, 2,   ZBTB10↑, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 2,   IL1↓, 1,   IL6↓, 3,   IL8↓, 1,   Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 5,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 10,   ChemoSen⇅, 1,   Dose↑, 3,   Dose↝, 1,   eff↓, 1,   eff↑, 6,   Half-Life↓, 2,   MDR1↓, 1,   P450↓, 1,   RadioS↑, 3,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 3,   p‑EGFR↓, 1,   EZH2↓, 1,   GutMicro↑, 1,   hTERT/TERT↓, 1,   IL6↓, 3,   LDH↑, 1,   Myc↓, 1,   TP53↓, 1,   TP53↑, 2,   TRIB3↑, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   AntiCan↑, 5,   AntiTum↑, 2,   cardioP↑, 2,   chemoP↑, 2,   hepatoP↑, 1,   Obesity↓, 2,   OS↑, 1,   Pin1↓, 1,   radioP↑, 2,   RenoP↑, 1,   Risk↓, 1,   TumVol↓, 1,  

Infection & Microbiome ⓘ

AntiFungal↑, 1,   Bacteria↓, 1,  
Total Targets: 238

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

TMAO↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↓, 2,   antiOx↑, 13,   Catalase↑, 3,   Ferroptosis↓, 1,   GPx↑, 4,   GSH↑, 7,   GSR↑, 1,   GSTs↑, 3,   H2O2↓, 1,   HDL↑, 1,   HNE↓, 1,   HO-1↑, 3,   Keap1↓, 1,   lipid-P↓, 6,   MDA↓, 6,   MPO↓, 2,   NADH↓, 1,   NRF2↑, 9,   RNS↓, 1,   ROS?, 1,   ROS↓, 19,   ROS↑, 5,   selenoP↑, 1,   SOD↑, 9,   TBARS↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   Insulin↓, 1,   mitResp↑, 2,   MMP↑, 2,  

Core Metabolism/Glycolysis ⓘ

Acetyl-CoA↑, 1,   ALAT↓, 3,   AMPK↑, 2,   p‑AMPK↑, 1,   CRM↑, 2,   glucose↓, 3,   GlucoseCon↑, 2,   glyC↓, 1,   H2S↑, 1,   LDH↓, 3,   LDH↑, 1,   LDL↓, 2,   NADPH↑, 1,   PPARα↝, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↓, 1,   BAX↓, 2,   Casp↓, 1,   Casp3↓, 1,   Casp9↓, 1,   Cyt‑c↓, 2,   Fas↓, 1,   Ferroptosis↓, 1,   iNOS↓, 2,   JNK↓, 1,   MAPK↓, 2,   TRPV1↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 2,   other↓, 2,   other↑, 4,   other↝, 7,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,   HSP70/HSPA5↑, 1,   HSPs↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 2,  

Migration ⓘ

5LO↓, 1,   AntiAg↓, 1,   AntiAg↑, 2,   Ca+2?, 1,   Ca+2↓, 1,   Ca+2↑, 2,   CLDN1↓, 1,   MMP9↓, 1,   TJ↓, 1,   TRPC1↓, 1,   ZO-1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   Hif1a↓, 1,   NO↓, 4,   NO↑, 1,  

Barriers & Transport ⓘ

BBB↓, 1,   BBB↑, 2,   GastroP↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 2,   COX2↓, 6,   CRP↓, 2,   CXCR4↓, 1,   IL17↓, 1,   IL18↓, 1,   IL1β↓, 2,   IL6↓, 6,   Imm↑, 3,   Inflam↓, 14,   Inflam↑, 1,   NF-kB↓, 5,   PGE2↓, 3,   TLR4↓, 1,   TNF-α↓, 5,  

Synaptic & Neurotransmission ⓘ

AChE↓, 5,   BChE↓, 1,   ChAT↑, 2,   tau↓, 1,  

Protein Aggregation ⓘ

AGEs↓, 1,   Aβ↓, 7,   BACE↓, 1,   NLRP3↓, 1,   NLRP3↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CYP19↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 5,   BioAv↑, 7,   BioAv↝, 4,   Dose⇅, 1,   Dose↝, 3,   eff↑, 8,   eff↝, 1,   Half-Life↓, 3,   Half-Life↝, 3,  

Clinical Biomarkers ⓘ

ALAT↓, 3,   ALP↓, 1,   AST↓, 4,   BP↓, 3,   creat↓, 1,   CRP↓, 2,   GutMicro↑, 3,   IL6↓, 6,   LDH↓, 3,   LDH↑, 1,   NOS2↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 3,   AntiCan↑, 2,   AntiDiabetic↑, 4,   cardioP↓, 1,   cardioP↑, 11,   cognitive↓, 2,   cognitive↑, 8,   hepatoP↑, 6,   memory↑, 9,   motorD↑, 1,   neuroP↑, 22,   Obesity↓, 2,   radioP↑, 1,   RenoP↑, 1,   toxicity↓, 2,   toxicity↝, 2,   toxicity∅, 1,   Weight↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 3,  
Total Targets: 149

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
3 Alpha-Lipoic-Acid
2 Capsaicin
1 Allicin (mainly Garlic)
1 Baicalein
1 Biochanin A
1 Boswellia (frankincense)
1 Celastrol
1 Chlorogenic acid
1 Choline
1 Curcumin
1 EGCG (Epigallocatechin Gallate)
1 Juglone
1 Luteolin
1 MCToil
1 Melatonin
1 Metformin
1 Pterostilbene
1 Quercetin
1 Resveratrol
1 Selenium NanoParticles
1 Spermidine
1 Thymol-Thymus vulgaris
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:38  Cells:%  prod#:%  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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