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 0Antioxidant
ROS">Rosmarinic acid 0Antioxidant
ROS">Citrate 00Neutral


NA, Not Available: Click to Expand ⟱
none (reserved)

Scientific Papers found: Click to Expand⟱
4542- AgNPs,    Silver Nanoparticles (AgNPs): Comprehensive Insights into Bio/Synthesis, Key Influencing Factors, Multifaceted Applications, and Toxicity─A 2024 Update
- Review, NA, NA
AntiCan↑, DNAdam↑, ATP↓, Apoptosis↑, ROS↓, TumCCA↑, *Bacteria↓, *BMD↑,
3456- ALA,    Renal-Protective Roles of Lipoic Acid in Kidney Disease
- Review, NA, NA
*RenoP↑, *ROS↓, *antiOx↑, *Inflam↓, *Sepsis↓, *IronCh↑, *BUN↓, *creat↓, *TNF-α↓, *IL6↓, *IL1β↓, *MDA↓, *NRF2↑, *HO-1↑, *NQO1↑, *chemoP↑, *eff↑, *NF-kB↓,
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↑,
3439- ALA,    The effect of alpha lipoic acid on the developmental competence of mouse isolated preantral follicles
- in-vitro, NA, NA
*ROS↓, *TAC↑, *eff↑, *SOD↑, *GPx↑, *Catalase↑, *GlucoseCon↑, *antiOx↑,
278- ALA,    The Multifaceted Role of Alpha-Lipoic Acid in Cancer Prevention, Occurrence, and Treatment
- Review, NA, NA
ROS↑, NRF2↑, Inflam↓, frataxin↑, *BioAv↓, ChemoSen↑, Hif1a↓, eff↑, FAK↓, ITGB1↓, MMP2↓, MMP9↓, EMT↓, Snail↓, Vim↓, Zeb1↓, P53↑, MGMT↓, Mcl-1↓, Bcl-xL↓, Bcl-2↓, survivin↓, Casp3↑, Casp9↑, BAX↑, p‑Akt↓, GSK‐3β↓, *antiOx↑, *ROS↓, selectivity↑, angioG↓, MMPs↓, NF-kB↓, ITGB3↓, NADPH↓,
1235- ALA,  Cisplatin,    α-Lipoic acid prevents against cisplatin cytotoxicity via activation of the NRF2/HO-1 antioxidant pathway
- in-vitro, Nor, HEI-OC1 - ex-vivo, NA, NA
ROS↑, HO-1↓, *toxicity↓, chemoP↑, *ROS↓, *HO-1↑, *SOD1↑, *NRF2↑,
931- And,    Effect of Andrographis Paniculata Aqueous Extract on Hyperammonemia Induced Alteration of Oxidative and Nitrosative Stress Factors in the Liver, Spleen and Kidney of Rats
- in-vivo, NA, NA
*SOD↝, *Catalase↝, *ROS↓, *MDA↓, *NO↓,
4279- Api,    The Beneficial Role of Apigenin against Cognitive and Neurobehavioural Dysfunction: A Systematic Review of Preclinical Investigations
- Review, NA, NA
*antiOx↑, *Inflam↓, *BBB↑, *5HT↑, *CREB↑, *BDNF↑, *memory↑, *motorD↑, *Mood↑, *cognitive↑, *ROS↓,
3392- ART/DHA,    Artemisinin inhibits inflammatory response via regulating NF-κB and MAPK signaling pathways
- in-vitro, Nor, Hep3B - in-vivo, NA, NA
*Inflam↓, *NF-kB↓, *ROS↓, *p‑p38↓, *p‑ERK↓,
3672- Ash,    Critical review of the Withania somnifera (L.) Dunal: ethnobotany, pharmacological efficacy, and commercialization significance in Africa
- Review, NA, NA
*cardioP↑, *antiOx↑, *ROS↓, *neuroP↑, *Inflam↓, *Apoptosis↓,
2614- Ba,    Therapeutic potentials of baicalin and its aglycone, baicalein against inflammatory disorders
- Review, NA, NA
*toxicity↓, *antiOx↑, *Inflam↓, *ROS↓, *NF-kB↓, *MCP1↓, *hepatoP↑, *neuroP↑,
1399- BBR,  Rad,    Radiotherapy Enhancing and Radioprotective Properties of Berberine: A Systematic Review
- Review, NA, NA
*ROS↓, *MDA↓, *TNF-α↓, *TGF-β↓, *IL10↑, ROS↑, DNAdam↑, mtDam↑, MMP↓, Apoptosis↑, TumCCA↑, Hif1a↓, VEGF↓, RadioS↑,
4273- BetA,    Betulinic acid, a natural PDE inhibitor restores hippocampal cAMP/cGMP and BDNF, improve cerebral blood flow and recover memory deficits in permanent BCCAO induced vascular dementia in rats
- in-vivo, NA, NA
*neuroP↑, *BDNF↑, *ROS↓, *Inflam↓, *cognitive↑,
3505- Bor,    Mineral requirements for mitochondrial function: A connection to redox balance and cellular differentiation
- Review, NA, NA
*glucose↓, *creat↓, *SOD↑, *MMP↑, *ROS↓,
3511- Bor,    Boron
- Review, NA, NA
*memory↑, *motorD↑, *neuroP↑, Ca+2↓, ATF4↑, NRF2↑, *Inflam↓, *ROS↓,
699- Bor,    Boric Acid Alleviates Gastric Ulcer by Regulating Oxidative Stress and Inflammation-Related Multiple Signaling Pathways
- in-vivo, NA, NA
*ROS↓, *MDA↓, *TNF-α↓, *IL6↓, *JAK2↓, *STAT3↓, *AMPK↑, *Sema3A/PlexinA1↑,
730- Bor,  Cisplatin,    The Effect of Boric Acid and Borax on Oxidative Stress, Inflammation, ER Stress and Apoptosis in Cisplatin Toxication and Nephrotoxicity Developing as a Result of Toxication
- in-vivo, NA, NA
*ROS↓, *Inflam↓, RenoP↑,
4264- CA,    Carnosic Acid Mitigates Depression-Like Behavior in Ovariectomized Mice via Activation of Nrf2HO-1 Pathway
- in-vivo, NA, NA
*NRF2↑, *HO-1↑, *Trx1↑, *BDNF↑, *5HT↑, *ROS↓, *TNF-α↓, *IL1β↓, *iNOS↓,
3871- Carno,    Unveiling the Hidden Therapeutic Potential of Carnosine, a Molecule with a Multimodal Mechanism of Action: A Position Paper
- Review, NA, NA
*ROS↓, *NO↓, *Inflam↓,
3890- Cin,    The Therapeutic Roles of Cinnamaldehyde against Cardiovascular Diseases
- Review, NA, NA
*cardioP↑, *Inflam↓, *ROS↓, *lipid-P↓, *AntiAg↑, *angioG↑, *GutMicro↑, *ER Stress↓,
1574- Citrate,    Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway
- in-vitro, Lung, A549 - in-vitro, Melanoma, WM983B - in-vivo, NA, NA
TumCG↓, eff↑, T-Cell↑, p‑IGF-1R↓, p‑Akt↓, PTEN↑, p‑eIF2α↑, OCR↓, ROS↓, ECAR∅, IL1↑, TNF-α↑, IL10↑, IGF-1R↓, eIF2α↑, PTEN↑, TCA↓, Glycolysis↓, selectivity↑, *toxicity∅, Dose∅,
3635- Cro,    A Review of Potential Efficacy of Saffron (Crocus sativus L.) in Cognitive Dysfunction and Seizures
- Review, NA, NA
*memory↑, *cognitive↑, *BioAv↑, *ROS↓, *IL1↓, *TNF-α↓, *NF-kB↓, *neuroP↑, *lipid-P↓, *Thiols↑, *antiOx↑, *AChE↓, *MAOA↝, *SIRT1↑, *PGC-1α↑, *Ach↑,
1510- CUR,  Chemo,    Combination therapy in combating cancer
- Review, NA, NA
*NRF2↑, *GSH↑, *ROS↓, ChemoSideEff↓, eff↑, OS↓, chemoP↑,
4177- DHA,    Dietary omega-3 fatty acids normalize BDNF levels, reduce oxidative damage, and counteract learning disability after traumatic brain injury in rats
- in-vivo, NA, NA
*BDNF↑, *CREB↑, *ROS↓, *cognitive↑,
3201- EGCG,    Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential
- Review, NA, NA
*AntiCan↑, *cardioP↑, *neuroP↑, *BioAv↝, *BioAv↓, *BioAv↓, *Dose↝, *Half-Life↝, *BioAv↑, *BBB↑, *hepatoP↓, *other↓, *Inflam↓, *NF-kB↓, *AP-1↓, *iNOS↓, *COX2↓, *ROS↓, *RNS↓, *IL8↓, *JAK↓, *PDGFR-BB↓, *IGF-1R↓, *MMP2↓, *P53↓, *NRF2↑, *TNF-α↓, *IL6↓, *E2Fs↑, *SOD1↑, *SOD2↑, Casp3↑, Cyt‑c↑, PARP↑, DNMTs↓, Telomerase↓, Hif1a↓, MMPs↓, BAX↑, Bak↑, Bcl-2↓, Bcl-xL↓, P53↑, PTEN↑, TumCP↓, MAPK↓, HGF/c-Met↓, TIMP1↑, HDAC↓, MMP9↓, uPA↓, GlutMet↓, ChemoSen↑, chemoP↑,
3211- EGCG,    Antioxidation Function of EGCG by Activating Nrf2/HO-1 Pathway in Mice with Coronary Heart Disease
- in-vivo, NA, NA
*cardioP↑, *VEGF↓, *MMP2↓, *SOD↑, *ROS↓, *HO-1↑, *NQO1↑, *NRF2↑,
1516- EGCG,    Epigallocatechin Gallate (EGCG): Pharmacological Properties, Biological Activities and Therapeutic Potential
- Review, NA, NA
*Dose∅, Half-Life∅, BioAv∅, BBB↑, toxicity∅, eff↓, Apoptosis↑, Casp3↑, Cyt‑c↑, cl‑PARP↑, DNMTs↓, Telomerase↓, angioG↓, Hif1a↓, NF-kB↓, MMPs↓, BAX↑, Bak↑, Bcl-2↓, Bcl-xL↓, P53↑, PTEN↑, IGF-1↓, H3↓, HDAC1↓, *LDH↓, *ROS↓,
4030- FulvicA,    Therapeutic Potential of Fulvic Acid in Chronic Inflammatory Diseases and Diabetes
- Review, NA, NA
*Inflam↓, TNF-α↓, *COX2↓, *PGE2↓, *ROS↓, *GutMicro↑, *BioEnh↑, *BioEnh↑, *SOD↑, *Catalase↑, *GPx↑,
1188- Gb,    The potential of Ginkgo biloba in the treatment of human diseases and the relationship to Nrf2-mediated antioxidant protection
- Review, NA, NA
*NRF2↑, *ROS↓,
2525- H2,    Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis
- in-vivo, NA, NA
OS↓, cardioP↑, *AST↓, ALAT↓, *ROS↓, *MDA↓, *hepatoP↑, *Inflam↓, chemoP↑,
2514- H2,    Hydrogen: A Novel Option in Human Disease Treatment
- Review, NA, NA
*Inflam↓, *IL1β↓, *IL6↓, *IL8↓, *IL10↓, *TNF-α↓, *ROS↓, *HO-1↓, *NRF2↑, *ER Stress↓, H2O2↑,
2507- H2,    Hydrogen protects against chronic intermittent hypoxia induced renal dysfunction by promoting autophagy and alleviating apoptosis
- in-vivo, NA, NA
*RenoP↑, *ROS↓, *Apoptosis↓, *ER Stress↓, *CHOP↓, *Casp12↓, *GRP78/BiP↓, *LC3‑Ⅱ/LC3‑Ⅰ↑, *Beclin-1↑, *p62↓, *mTOR↓,
4345- H2,    The Benefit of Hydrogen Gas as an Adjunctive Therapy for Chronic Obstructive Pulmonary Disease
- Human, NA, NA
*Inflam↓, *antiOx↑, *ROS↓, *NLRP3↑, *NF-kB↓, *SOD↑, *Catalase↑, *AntiAg↑,
4237- H2,    Hydrogen-Rich Saline Protects Against Spinal Cord Injury in Rats
- in-vitro, NA, NA
*Apoptosis↓, *ROS↓, *motorD↑, *BDNF↑,
1633- HCA,    Hydroxycitric Acid Alleviated Lung Ischemia-Reperfusion Injury by Inhibiting Oxidative Stress and Ferroptosis through the Hif-1α Pathway
- in-vivo, NA, NA - in-vitro, Nor, HUVECs
*other↓, *Inflam↓, *MDA↓, *ROS↓, *Iron↓, *SOD↓, *Hif1a↓, *HO-1↓,
4213- Hup,    Huperzine A-Liposomes Efficiently Improve Neural Injury in the Hippocampus of Mice with Chronic Intermittent Hypoxia
- in-vivo, NA, NA
*cognitive↑, *SOD↑, *GPx↑, *MDA↓, *ROS↓, *Iron↓, *TfR1/CD71↓, *FTL↓, *ERK↑, *PKA↑, *CREB↑, *BDNF↑, *PSD95↑, *neuroP↑,
4209- Hup,    Huperzine A, reduces brain iron overload and alleviates cognitive deficit in mice exposed to chronic intermittent hypoxia
- in-vivo, NA, NA
*ROS↓, *cognitive↑, *neuroP↑, *Bax:Bcl2↓, *Casp3↑, *NADPH↓, *NOX↓, *TfR1/CD71↓, *Iron↓, *PSD95↑, *BDNF↑,
4339- LT,    Luteolin inhibits GPVI-mediated platelet activation, oxidative stress, and thrombosis
- in-vivo, NA, NA
*AntiAg↑, *ROS↓,
4338- LT,    Luteolin: a natural product with multiple mechanisms for atherosclerosis
- Review, NA, NA
*Inflam↓, *ROS↓, *PDGF↓, *lipid-P↓, *AMPK↑, *SIRT1↑, *AntiAg↑,
2905- LT,    Luteolin blocks the ROS/PI3K/AKT pathway to inhibit mesothelial-mesenchymal transition and reduce abdominal adhesions
- in-vivo, NA, HMrSV5
*ROS↓, *p‑Akt↓, *Vim↓, *E-cadherin↑, *PI3K↓,
2544- M-Blu,    Methylene blue and its importance in medicine
- Review, NA, NA
*ROS↓, antiOx↑, BBB↑, neuroP↑, GSR↓, tau↓,
1776- MEL,    Therapeutic strategies of melatonin in cancer patients: a systematic review and meta-analysis
- Review, NA, NA
Remission↑, OS↑, neuroP↑, VEGF↓, KISS1↑, TumCP↓, ChemoSideEff↓, radioP↑, Dose∅, *ROS↓, DNArepair↑, ROS↑,
1777- MEL,    Melatonin as an antioxidant: under promises but over delivers
- Review, NA, NA
*ROS↓, *Fenton↓, *antiOx↑, *toxicity∅, *GPx↑, *GSR↑, *GSH↑, *NO↓, *Iron↓, *Copper↓, *IL1β↓, *iNOS↓, *Casp3↓, *BBB↑, *RenoP↑, chemoP↑, *Ca+2↝, eff↑, *PKCδ?, ChemoSen↑, eff↑, Akt↓, DR5↑, selectivity↑, ROS↑, eff↑,
4116- MF,    Low‑frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury
- in-vivo, NA, NA
*Inflam↓, *TNF-α↓, *IL1β↓, *iNOS↓, *ROS↓, *Catalase↑, *SOD↑, HSP70/HSPA5↑,
3468- MF,    An integrative review of pulsed electromagnetic field therapy (PEMF) and wound healing
- Review, NA, NA
*other↑, *necrosis↓, *IL6↑, *TGF-β↑, *iNOS↑, *MMP2↑, *MCP1↑, *HO-1↑, *Inflam↓, *IL1β↓, *IL6↓, *TNF-α↓, *BioAv↑, eff⇅, DNAdam↑, Apoptosis↑, ROS↑, TumCP↓, *ROS↓, *FGF↑,
209- MFrot,  MF,    The effect of a rotating magnetic field on the antioxidant system in healthy volunteers - preliminary study
- Human, NA, NA
*SOD↑, *Catalase↑, *ROMO1↑, *MDA↓, *TAC↑, *ROS↓,
3844- Moringa,    Review of the Safety and Efficacy of Moringa oleifera
- Review, NA, NA
*antiOx↑, *RenoP↑, *hepatoP↑, *radioP↑, *eff↑, *toxicity↓, *ROS↓, *lipid-P↓, *DNAdam↓, *Catalase↑, *SOD↑, *GPx↑, *GSR↑, *GSTs↑, *AST↓, *ALAT↓, *ALP↓, *Bil↓,
3850- MSM,    The Influence of Methylsulfonylmethane on Inflammation-Associated Cytokine Release before and following Strenuous Exercise
- Human, NA, NA
*Inflam↓, *IL1β↓, *NF-kB↓, *NLRP3↓, *ROS↓,
3810- mushLions,    Key Mechanisms and Potential Implications of Hericium erinaceus in NLRP3 Inflammasome Activation by Reactive Oxygen Species during Alzheimer’s Disease
- Review, NA, NA
*neuroP↑, *p‑tau↓, *APP↓, *Aβ↓, *ROS↓, *Inflam↓, *NLRP3↓,
3808- mushLions,    Neuroprotective Metabolites of Hericium erinaceus Promote Neuro-Healthy Aging
- in-vitro, NA, NA
*Inflam↓, *ROS↓, *neuroP↑,

Showing Research Papers: 1 to 50 of 85
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 85

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

antiOx↑, 1,   frataxin↑, 1,   GSR↓, 1,   H2O2↑, 1,   HO-1↓, 1,   NRF2↑, 2,   ROS↓, 2,   ROS↑, 6,  

Mitochondria & Bioenergetics

ATP↓, 1,   MMP↓, 1,   mtDam↑, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis

ALAT↓, 1,   ECAR∅, 1,   GlutMet↓, 1,   Glycolysis↓, 1,   NADPH↓, 1,   TCA↓, 1,  

Cell Death

Akt↓, 1,   p‑Akt↓, 2,   Apoptosis↑, 4,   Bak↑, 2,   BAX↑, 3,   Bcl-2↓, 3,   Bcl-xL↓, 3,   Casp3↑, 3,   Casp9↑, 1,   Cyt‑c↑, 2,   DR5↑, 1,   HGF/c-Met↓, 1,   MAPK↓, 1,   Mcl-1↓, 1,   survivin↓, 1,   Telomerase↓, 2,  

Transcription & Epigenetics

H3↓, 1,   KISS1↑, 1,  

Protein Folding & ER Stress

eIF2α↑, 1,   p‑eIF2α↑, 1,   HSP70/HSPA5↑, 1,  

DNA Damage & Repair

DNAdam↑, 3,   DNArepair↑, 1,   DNMTs↓, 2,   MGMT↓, 1,   P53↑, 3,   PARP↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State

EMT↓, 1,   GSK‐3β↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   IGF-1↓, 1,   IGF-1R↓, 1,   p‑IGF-1R↓, 1,   PTEN↑, 4,   TumCG↓, 1,  

Migration

Ca+2↓, 1,   FAK↓, 1,   ITGB1↓, 1,   ITGB3↓, 1,   MMP2↓, 1,   MMP9↓, 2,   MMPs↓, 3,   Snail↓, 1,   TIMP1↑, 1,   TumCP↓, 3,   uPA↓, 1,   Vim↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature

angioG↓, 2,   ATF4↑, 1,   Hif1a↓, 4,   VEGF↓, 2,  

Barriers & Transport

BBB↑, 2,  

Immune & Inflammatory Signaling

IL1↑, 1,   IL10↑, 1,   Inflam↓, 1,   NF-kB↓, 2,   T-Cell↑, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Synaptic & Neurotransmission

tau↓, 1,  

Drug Metabolism & Resistance

BioAv∅, 1,   ChemoSen↑, 3,   Dose∅, 2,   eff↓, 1,   eff↑, 6,   eff⇅, 1,   Half-Life∅, 1,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers

ALAT↓, 1,  

Functional Outcomes

AntiCan↑, 1,   cardioP↑, 1,   chemoP↑, 5,   ChemoSideEff↓, 2,   neuroP↑, 2,   OS↓, 2,   OS↑, 1,   radioP↑, 1,   Remission↑, 1,   RenoP↑, 1,   toxicity∅, 1,  
Total Targets: 103

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 11,   Bil↓, 1,   Catalase↑, 6,   Catalase↝, 1,   Copper↓, 1,   Fenton↓, 1,   GPx↑, 5,   GSH↑, 3,   GSR↑, 2,   GSTs↑, 1,   HO-1↓, 2,   HO-1↑, 5,   Iron↓, 4,   lipid-P↓, 5,   MDA↓, 8,   NQO1↑, 2,   NRF2↑, 9,   RNS↓, 1,   ROMO1↑, 1,   ROS↓, 48,   ROS↑, 1,   SOD↓, 1,   SOD↑, 9,   SOD↝, 1,   SOD1↑, 2,   SOD2↑, 1,   TAC↑, 2,   Thiols↑, 1,   Trx1↑, 1,  

Metal & Cofactor Biology

FTL↓, 1,   IronCh↑, 2,   TfR1/CD71↓, 2,  

Mitochondria & Bioenergetics

MMP↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis

Acetyl-CoA↑, 1,   ALAT↓, 1,   AMPK↑, 2,   BUN↓, 1,   CREB↑, 3,   glucose↓, 1,   GlucoseCon↑, 2,   LDH↓, 1,   NADPH↓, 1,   SIRT1↑, 2,  

Cell Death

p‑Akt↓, 1,   Apoptosis↓, 3,   Bax:Bcl2↓, 1,   Casp12↓, 1,   Casp3↓, 1,   Casp3↑, 1,   iNOS↓, 4,   iNOS↑, 1,   necrosis↓, 1,   p‑p38↓, 1,  

Transcription & Epigenetics

Ach↑, 2,   other↓, 2,   other↑, 1,  

Protein Folding & ER Stress

CHOP↓, 1,   ER Stress↓, 3,   GRP78/BiP↓, 1,  

Autophagy & Lysosomes

Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   p62↓, 1,  

DNA Damage & Repair

DNAdam↓, 1,   P53↓, 1,  

Cell Cycle & Senescence

E2Fs↑, 1,  

Proliferation, Differentiation & Cell State

ERK↑, 1,   p‑ERK↓, 1,   FGF↑, 1,   IGF-1R↓, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration

AntiAg↑, 4,   AP-1↓, 1,   APP↓, 1,   Ca+2↝, 1,   E-cadherin↑, 1,   MMP2↓, 2,   MMP2↑, 1,   PDGF↓, 1,   PKA↑, 1,   PKCδ?, 1,   Sema3A/PlexinA1↑, 1,   TGF-β↓, 1,   TGF-β↑, 1,   Vim↓, 1,  

Angiogenesis & Vasculature

angioG↑, 1,   Hif1a↓, 1,   NO↓, 3,   PDGFR-BB↓, 1,   VEGF↓, 1,  

Barriers & Transport

BBB↑, 3,  

Immune & Inflammatory Signaling

COX2↓, 2,   IL1↓, 1,   IL10↓, 1,   IL10↑, 1,   IL1β↓, 7,   IL6↓, 5,   IL6↑, 1,   IL8↓, 2,   Inflam↓, 23,   JAK↓, 1,   JAK2↓, 1,   MCP1↓, 1,   MCP1↑, 1,   NF-kB↓, 7,   PGE2↓, 1,   TNF-α↓, 9,  

Cellular Microenvironment

NOX↓, 1,  

Synaptic & Neurotransmission

5HT↑, 2,   AChE↓, 1,   BDNF↑, 7,   ChAT↑, 1,   MAOA↝, 1,   PSD95↑, 2,   p‑tau↓, 1,  

Protein Aggregation

Aβ↓, 1,   NLRP3↓, 2,   NLRP3↑, 1,  

Drug Metabolism & Resistance

BioAv↓, 3,   BioAv↑, 3,   BioAv↝, 1,   BioEnh↑, 2,   Dose↝, 1,   Dose∅, 1,   eff↑, 3,   Half-Life↝, 1,  

Clinical Biomarkers

ALAT↓, 1,   ALP↓, 1,   AST↓, 2,   Bil↓, 1,   BMD↑, 1,   creat↓, 2,   GutMicro↑, 2,   IL6↓, 5,   IL6↑, 1,   LDH↓, 1,  

Functional Outcomes

AntiAge↑, 1,   AntiCan↑, 2,   cardioP↑, 5,   chemoP↑, 1,   cognitive↑, 7,   hepatoP↓, 1,   hepatoP↑, 3,   memory↑, 4,   Mood↑, 1,   motorD↑, 3,   neuroP↑, 11,   radioP↑, 1,   RenoP↑, 4,   toxicity↓, 3,   toxicity∅, 2,   Weight↓, 1,  

Infection & Microbiome

Bacteria↓, 1,   Sepsis↓, 1,  
Total Targets: 156

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
6 Hydrogen Gas
5 Alpha-Lipoic-Acid
5 Silymarin (Milk Thistle) silibinin
4 Boron
4 Thymoquinone
3 EGCG (Epigallocatechin Gallate)
3 Luteolin
3 Magnetic Fields
3 Vitamin C (Ascorbic Acid)
2 Silver-NanoParticles
2 Cisplatin
2 Radiotherapy/Radiation
2 Chemotherapy
2 Huperzine A/Huperzia serrata
2 Melatonin
2 Mushroom Lion’s Mane
2 Phenylbutyrate
2 Propolis -bee glue
2 Quercetin
2 Resveratrol
2 Rosmarinic acid
2 Selenium NanoParticles
1 Andrographis
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Ashwagandha(Withaferin A)
1 Baicalein
1 Berberine
1 Betulinic acid
1 Carnosic acid
1 Carnosine
1 Cinnamon
1 Citric Acid
1 Crocetin
1 Curcumin
1 Docosahexaenoic Acid
1 Shilajit/Fulvic Acid
1 Ginkgo biloba
1 HydroxyCitric Acid
1 Methylene blue
1 Magnetic Field Rotating
1 Moringa oleifera
1 Methylsulfonylmethane
1 N-Acetyl-Cysteine
1 5-fluorouracil
1 sericin
1 Propyl gallate
1 Rutin
1 Orlistat
1 chitosan
1 Sesame seeds and Oil
1 Sulforaphane (mainly Broccoli)
1 Gemcitabine (Gemzar)
1 Silicic Acid
1 Shikonin
1 Squalene
1 Safflower yellow
1 Taurine
1 doxorubicin
1 Vitamin A, Retinoic Acid
1 Vitamin D3
1 Vitamin E
1 Vitamin B3,Niacin
1 Vitamin K2
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:0  Cells:%  prod#:%  Target#:275  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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