buckwheat sprouts / ROS Cancer Research Results

BuckWS, buckwheat sprouts: Click to Expand ⟱
Features:

Buckwheat Sprouts — edible young seedlings produced by germination of buckwheat, principally common buckwheat (Fagopyrum esculentum) and Tartary buckwheat (Fagopyrum tataricum). They are a flavonoid- and polyphenol-rich functional food rather than a standardized drug or single-molecule therapeutic. Common buckwheat sprouts characteristically contain rutin, orientin, isoorientin, vitexin, isovitexin, quercetin-related glycosides, chlorogenic acid and other phenolic compounds, whereas Tartary buckwheat sprouts are generally more rutin-dominant and can contain substantially higher rutin concentrations. Germination markedly alters the phytochemical profile relative to ungerminated grain. Composition varies with species, sprouting duration, illumination, cultivar and cultivation conditions. Buckwheat sprouts also contain the phototoxic naphthodianthrone derivatives fagopyrins, making excessive consumption of green sprouts potentially more problematic than consumption of buckwheat grain.

Primary mechanisms (ranked):

  1. Polyphenol/flavonoid-mediated redox modulation, including direct radical scavenging, inhibition of lipid oxidation and enhancement of endogenous antioxidant defenses.
  2. Suppression of inflammatory NF-κB/MAPK signaling with reduced iNOS, COX-2, TNF-α, IL-6 and related inflammatory mediators.
  3. NRF2/KEAP1 antioxidant-response activation, demonstrated particularly with Tartary buckwheat sprout polyphenol extracts, increasing HO-1, NQO1, SOD, CAT and GST.
  4. Metabolic and vascular modulation attributable to rutin, flavonoids, GABA and other sprout constituents, including effects on lipid metabolism and, particularly after fermentation, ACE-related blood-pressure regulation.
  5. Potential antiproliferative and cytotoxic effects of concentrated buckwheat polyphenol preparations in cancer-cell models; direct anticancer evidence for ordinary dietary buckwheat sprouts remains substantially weaker than evidence for isolated constituent flavonoids or concentrated extracts.

Bioavailability / PK relevance: Buckwheat sprouts are a complex food matrix and do not have a single definable pharmacokinetic profile. Rutin has relatively poor absorption as intact rutin and largely reaches the colon, where microbial metabolism produces quercetin and other metabolites that subsequently enter the circulation. Human pharmacokinetic studies demonstrate delayed and highly variable systemic exposure after rutin-containing foods. The C-glycosyl flavones orientin, isoorientin, vitexin and isovitexin contribute additional exposure but their concentrations vary substantially among sprout preparations. Consequently, phytochemical content cannot be directly converted into systemic therapeutic exposure.

In-vitro vs systemic exposure relevance: Concentrated methanolic, ethanolic, polyphenol-rich or subcritical-water sprout extracts used in many cell studies can produce concentrations substantially different from those achievable by eating ordinary fresh sprouts. Cancer-cell and mechanistic extract studies should therefore not be interpreted as demonstrating equivalent systemic anticancer activity from dietary consumption. Food-level effects are more plausibly mediated by repeated intestinal exposure, metabolites and modulation of antioxidant, inflammatory and metabolic pathways.

Clinical evidence status: Predominantly preclinical and nutritional. Evidence includes compositional studies, biochemical assays, cultured-cell studies and animal models of inflammation, oxidative stress, dyslipidemia and hypertension. Direct randomized human therapeutic trials of buckwheat sprouts themselves are sparse or absent in the literature identified, and there is no established clinical anticancer indication. Buckwheat sprouts should therefore be classified as a functional food / preclinical nutraceutical rather than an established treatment. Safety is generally compatible with food use, but large or repetitive consumption of green sprouts may increase fagopyrin exposure and risk of photosensitization; one experimental assessment proposed keeping fresh sprout intake below approximately 40 g/day, although a validated human toxicological threshold has not been established.

Major Bioactive Ingredients in Buckwheat Sprouts

Ingredient Class Relative Importance Peak Sprout Age Content at Peak Notes
Isoorientin C-glycosyl flavone Major Day 3(debatable) 5.8 mg/100 g fresh weight Peaks early during sprout development and subsequently declines. One of the characteristic luteolin C-glycosides of common buckwheat sprouts.
Orientin C-glycosyl flavone Major Day 3(debatable) 11.7 mg/100 g fresh weight Peaks early during sprout development and subsequently declines. Characteristic luteolin C-glycoside.
Isovitexin C-glycosyl flavone Major Day 3(debatable) 26.2 mg/100 g fresh weight One of the most abundant C-glycosyl flavones in young common buckwheat sprouts. Concentration declines as sprouts mature.
Vitexin C-glycosyl flavone Major Day 3(debatable) 28.9 mg/100 g fresh weight Highest of the four measured C-glycosyl flavones at day 3 in the referenced growth study. Declines substantially by day 10.
Rutin Flavonol glycoside Major Day 6 109.0 mg/100 g fresh weight Unlike the C-glycosyl flavones, rutin continues increasing after day 3 and reaches a pronounced fresh-weight maximum around day 6 before declining. Especially abundant in Tartary buckwheat.
Quercetin-3-O-robinobioside Flavonol glycoside Major to moderate Not clearly established Variable Characteristic flavonol glycoside of common buckwheat sprouts. Available studies confirm its presence but do not establish a consistent developmental peak comparable with the five major phenols above.
Quercetin Flavonol Moderate Species-dependent Variable More prominent in some Tartary buckwheat preparations. Germination-time behavior differs by cultivar and species, so a single optimal harvest day should not be assigned.
Chlorogenic acid Phenolic acid Moderate Not clearly established Variable Important non-flavonoid phenolic constituent, but a reproducible peak harvest age is not sufficiently established.

Harvest interpretation: Approximately day 3 favors maximum concentrations of the C-glycosyl flavones isoorientin, orientin, isovitexin and vitexin. Approximately day 6 provides a better overall compromise because rutin and total measured phenols peak at this stage. In one common buckwheat study, total phenols reached 162.9 mg/100 g fresh weight at day 6.
-in common buckwheat, orientin, isoorientin, vitexin, and isovitexin are reported at their highest concentrations in the cotyledons.
-***other study claims "In the edible parts of common buckwheat sprouts, individual phenolics significantly increased during sprout growth from 6 to 10 days after sowing (DAS), whereas in tartary buckwheat sprouts they did not." ****

Tartary Buckwheat Sprout Flour Compared with Fresh Sprouts

Form Rutin Potential Other Flavonoids Main Advantages Main Limitations Overall Interpretation
Fresh Tartary buckwheat sprouts High; commonly about 20–50+ mg/g dry weight Present, but rutin is usually dominant Least processed; retains fresh plant matrix; no drying-related degradation High water content; perishable; larger serving required for equivalent dry-matter intake Excellent whole-food source, especially for rutin
Tartary buckwheat sprout flour or powder High; approximately 20–50+ mg/g powder may be achievable depending on cultivar and processing Retained to varying degrees depending on drying method Concentrated; shelf-stable; easy to measure and consume; substantially less volume than fresh sprouts Processing can reduce flavonoids; quality depends strongly on drying temperature and storage Potentially nearly as useful as fresh sprouts for rutin if gently dried
Freeze-dried Tartary buckwheat sprout powder Very high retention expected Generally better preserved than with high-temperature drying Excellent phytochemical preservation; concentrated and stable More expensive; product availability may be limited Preferred dried formulation when maximum flavonoid retention is the objective
Hot-air-dried Tartary buckwheat sprout flour High if dried under controlled moderate temperatures Moderate to high retention Lower cost than freeze drying; practical for commercial production Heat can reduce rutin and other phenolics; retention depends on temperature and duration Good option when drying is performed at approximately 50–70°C rather than high baking temperatures
Tartary buckwheat grain flour Moderate; commonly much lower than sprout flour Different profile from sprouted material Cheap; widely available; easy to incorporate into foods Not equivalent to sprout flour; substantially lower rutin in many comparisons Useful food ingredient but inferior to true sprout flour for concentrated rutin delivery
Common buckwheat sprouts or microgreens Lower than Tartary buckwheat Richer balanced mixture of orientin, isoorientin, vitexin and isovitexin Broader flavonoid profile; useful complement to Tartary buckwheat Lower rutin concentration Potentially preferable when the objective is broad C-glycosyl flavone exposure rather than maximum rutin

Practical interpretation: Tartary buckwheat sprout flour is a concentrated and convenient alternative to fresh sprouts, particularly when rutin is the primary target. Freeze-dried or gently dried sprout powder is preferable because excessive heat can reduce flavonoid content. Sprout flour should not be confused with ordinary Tartary buckwheat grain flour, which generally contains substantially less rutin.

Buckwheat Sprout Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells Primary Effect Notes / Interpretation
1 Oxidative stress and antioxidant defense ROS ↓ (context-dependent) ROS ↓; antioxidant capacity ↑ Redox protection Sprout extracts scavenge radicals, inhibit lipid oxidation and reduce intracellular peroxide and superoxide. Unlike many cytotoxic anticancer agents, the dominant sprout-level evidence is antioxidant rather than pro-oxidant.
2 NF-κB inflammatory signaling NF-κB ↓ NF-κB ↓ Anti-inflammatory signaling Buckwheat sprout extracts inhibit NF-κB p65 nuclear translocation and inflammatory mediator production in macrophage and inflammatory models.
3 NRF2 KEAP1 antioxidant response NRF2 ↑ NRF2 ↑ (model-dependent) Induction of endogenous antioxidant enzymes Tartary buckwheat sprout polyphenol extract promoted NRF2 nuclear translocation with HO-1, NQO1, SOD, CAT and GST induction in oxidatively stressed HepG2 cells.
4 COX-2 and iNOS inflammatory mediators COX-2 ↓; iNOS ↓ COX-2 ↓; iNOS ↓ Reduced inflammatory mediator synthesis Observed principally in LPS-stimulated macrophage/extract models.
5 Pro-inflammatory cytokines IL-6 ↓; TNF-α ↓ IL-6 ↓; TNF-α ↓ Anti-inflammatory effect Supported by macrophage studies and oral administration of sprout extract in inflammatory mouse models.
6 MAPK inflammatory signaling MAPK phosphorylation ↓ MAPK phosphorylation ↓ Inflammatory signal suppression Especially documented for flavonoid-rich Tartary buckwheat sprout preparations.
7 Mitochondrial redox homeostasis Mitochondrial membrane potential normalization Mitochondrial protection (model-dependent) Protection against oxidative mitochondrial dysfunction Demonstrated in H2O2-stressed HepG2 cells; this is cytoprotective rather than evidence of selective cancer-cell mitochondrial toxicity.
8 Lipid metabolism Not established Triglycerides ↓ (animal models) Metabolic modulation Sprout preparations have improved selected lipid endpoints in animal studies, but findings depend strongly on sprout processing and diet model.
9 ACE and vascular signaling Not established ACE ↓; vasorelaxation ↑ Potential blood-pressure reduction Strongest evidence applies to fermented buckwheat sprouts and fermentation-derived peptides rather than ordinary fresh sprouts.
10 Cancer cell proliferation and viability Viability ↓ (high concentration only) Not established Potential cytotoxicity Reported mainly for concentrated polyphenol extracts. Ordinary dietary sprout intake has not been shown to achieve comparable systemic exposure.
11 Clinical Translation Constraint Dietary exposure far below many extract-study conditions Variable phytochemical exposure Limits therapeutic extrapolation Species, sprouting age, lighting and extraction strongly alter flavonoid content. Rutin has low and delayed oral bioavailability. Fagopyrin exposure and potential phototoxicity limit indiscriminate high-dose green-sprout consumption.


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)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"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


Scientific Papers found: Click to Expand⟱
7957- BuckWS,    Improving the antioxidant activity of buckwheat (Fagopyrum tataricm Gaertn) sprout with trace element water
- Study, Nor, NA
*Dose↑, *eff↑, *eff↝, *ROS↓, *IronCh↑, *SOD↑, *lipid-P↓,
7955- BuckWS,    Buckwheat (Fagopyrum esculentum M.) Sprout Treated with Methyl Jasmonate (MeJA) Improved Anti-Adipogenic Activity Associated with the Oxidative Stress System in 3T3-L1 Adipocytes
- in-vitro, Nor, 3T3
*eff↑, *ROS↓, *lipid-P↓,
7946- BuckWS,    Extract of buckwheat sprouts scavenges oxidation and inhibits pro-inflammatory mediators in lipopolysaccharide-stimulated macrophages (RAW264.7)
- Study, Nor, NA
*ROS↓, *IronCh↑, *IL6↓, *TNF-α↓, *iNOS↓, *COX2/PTGS2↓,
7944- BuckWS,    Extracts from Tartary Buckwheat Sprouts Restricts Oxidative Injury Induced by Hydrogen Peroxide in HepG2 by Upregulating the Redox System
- in-vitro, Nor, HepG2
*ROS↓, *MMP↑, *TAC↑, *SOD↑, *Catalase↑, *GSTA1↑, *NRF2↑, *NQO1↑, *HO-1↑,
7951- RT,  BuckWS,    The anticancer potential of the dietary polyphenol rutin: Current status, challenges, and perspectives
- Review, Nor, NA
*Dose↝, *BioAv↓, *BioAv↓, *BioAv↓, *BioAv↓, *BioAv↝, TumCP↓, Risk↓, *radioP↑, chemoPv↑, TumCCA↑, GSK‐3β↑, Wnt↓, β-catenin/ZEB1↓, ROS↑, BAX↑, Casp3↑, Casp8↑, Casp9↑, PARP↑, Beclin-1/ATG6↑, ATG5↑, LC3II↑, DNMT1↓, P21↑, CDK1↑, CycB/CCNB1↓, TNF-α↑, VEGF↓, IL1β↓, NF-kB↓, AP-1↓, MYCN↓, AMPK↑, MAPK↓, PI3K↓, Akt↓, cMET↓, P-gp/ABCB1↓, MRP1/ABCC1↓, ABCG2↓, MMPs↓, TNF-α↓, iNOS↓, COX2/PTGS2↓, angioG↓, STAT3↓, *chemoP↑, *ROS↓, *MDA↓, *P53↓, *Casp3↓, *Casp9↓, *JNK↓, *TNF-α↓, *p38↓, *MAPK↓, GSH↓, ChemoSen↑, *hepatoP↑, *COX1↓, *COX2/PTGS2↓, *15-LOX/ALOX15↓, RenoP↑, *toxicity↓,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

MYCN↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   ROS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   BAX↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   iNOS↓, 1,   MAPK↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   LC3II↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNMT1↓, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↑, 1,   CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cMET↓, 1,   GSK‐3β↑, 1,   PI3K↓, 1,   STAT3↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   MMPs↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1β↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABCG2↓, 1,   ChemoSen↑, 1,   MRP1/ABCC1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,   RenoP↑, 1,   Risk↓, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

15-LOX/ALOX15↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   GSTA1↑, 1,   HO-1↑, 1,   lipid-P↓, 2,   MDA↓, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 5,   SOD↑, 2,   TAC↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1,  

Cell Death(tgid=5) ⓘ

Casp3↓, 1,   Casp9↓, 1,   iNOS↓, 1,   JNK↓, 1,   MAPK↓, 1,   p38↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2/PTGS2↓, 2,   IL6↓, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↝, 1,   Dose↑, 1,   Dose↝, 1,   eff↑, 2,   eff↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,   hepatoP↑, 1,   radioP↑, 1,   toxicity↓, 1,  
Total Targets: 35

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
5 buckwheat sprouts
1 Rutin
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#:470  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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