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


Nor, Normal Healthy: Click to Expand ⟱
Normal Healthy
Scientific Papers found: Click to Expand⟱
4113- ,    ROS_levels_in_H2O2-treated_Glioblastoma_Cell_Line">Post-exposure Effects of PEMF on ROS levels in H2O2-treated Glioblastoma Cell Line
- in-vitro, Nor, U87MG
*ROS↓, *SOD2↑,
1406- AgNPs,    The antioxidant effects of silver, gold, and zinc oxide nanoparticles on male mice in in vivo condition
- in-vivo, Nor, NA
*ROS↓, *GPx↑, *Catalase↑, *ROS↑,
4434- AgNPs,  SSE,    Sodium Selenite Ameliorates Silver Nanoparticles Induced Vascular Endothelial Cytotoxic Injury by Antioxidative Properties and Suppressing Inflammation Through Activating the Nrf2 Signaling Pathway
- vitro+vivo, Nor, NA
*ROS↓, *Inflam↓, *NLRP3↓, *NF-kB↓, *NRF2↑, *HO-1↑, *toxicity↓,
4447- AgNPs,    Anti-inflammatory action of silver nanoparticles in vivo: systematic review and meta-analysis
- Review, Nor, NA
*Inflam↓, *COX2↓, *ROS↓, *Dose↝, *eff↑, *toxicity↓, *IL4↑, *IL5↑, *IL10↑, *IL1↓, *IL6↓, *TNF-α↓, *NF-kB↓, *MDA↓, *GSH↑,
2206- AgNPs,  RES,    ENHANCED EFFICACY OF RESVERATROL-LOADED SILVER NANOPARTICLE IN ATTENUATING SEPSIS-INDUCED ACUTE LIVER INJURY: MODULATION OF INFLAMMATION, OXIDATIVE STRESS, AND SIRT1 ACTIVATION
- in-vivo, Nor, NA
*hepatoP↑, *Inflam↓, *NF-kB↓, *VEGF↓, *SIRT1↑, *ROS↓, *Dose↝, *Catalase↑, *MDA↓, *MPO↓, *NO↓, *ALAT↓, *AST↓, *antiOx↑,
2661- AL,    Allicin alleviates traumatic brain injury-induced neuroinflammation by enhancing PKC-δ-mediated mitophagy
- in-vivo, Nor, NA
*TNF-α↓, *IL1β↓, *IL6↓, *ROS↓, *NLRP3↓, *TLR4↓, *PKCδ↑, neuroP↑,
3451- ALA,    Alpha-lipoic acid ameliorates H2O2-induced human vein endothelial cells injury via suppression of inflammation and oxidative stress
- in-vitro, Nor, HUVECs
*LDH↓, *NOX4↓, *NF-kB↓, *iNOS↓, *VCAM-1↓, *ICAM-1↓, *ROS↓, *cardioP↑,
3446- ALA,  CUR,    The Potential Protective Effect of Curcumin and α-Lipoic Acid on N-(4-Hydroxyphenyl) Acetamide-induced Hepatotoxicity Through Downregulation of α-SMA and Collagen III Expression
- in-vivo, Nor, NA
*hepatoP↑, *α-SMA↓, *COL3A1↓, *ROS↓, *GSH↑, *ALAT↓, *AST↓, *ALP↓, *MDA↓,
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↑,
1347- And,    Suppression of rat neutrophil reactive oxygen species production and adhesion by the diterpenoid lactone andrographolide
- in-vitro, Nor, NA
*ROS↓,
2318- Api,    Apigenin as a multifaceted antifibrotic agent: Therapeutic potential across organ systems
- Review, Nor, NA
*ROS↓, *PKM2↓, *Hif1a↓, *TGF-β↓, *AMPK↑, *Inflam↓, *PI3K↓, *Akt↑, *NRF2↑, *NF-kB↓,
2317- Api,    Apigenin intervenes in liver fibrosis by regulating PKM2-HIF-1α mediated oxidative stress
- in-vivo, Nor, NA
*hepatoP↑, *PKM2↓, *Hif1a↓, *MDA↓, *Catalase↓, *GSH↑, *SOD↑, *GPx↑, *TAC↑, *α-SMA↓, *Vim↓, *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↓,
4991- ART/DHA,  doxoR,    Dihydroartemisinin alleviates doxorubicin-induced cardiotoxicity and ferroptosis by activating Nrf2 and regulating autophagy
- in-vivo, Nor, H9c2
*cardioP↑, *ROS↓, *Ferroptosis↓, *NRF2↑, Keap1↓,
4810- ASTX,    Effects of Astaxanthin on the Proliferation and Migration of Breast Cancer Cells In Vitro
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
TumCP↓, TumCMig↓, selectivity↑, *BDNF↑, *ROS↓, *TNF-α↓, *IL6↓, *IFN-γ↓, *NF-kB↓, BAX⇅, Bcl-2↓, *antiOx↑, radioP↑, ChemoSen↑,
5418- ASTX,    Astaxanthin supplementation mildly reduced oxidative stress and inflammation biomarkers: a systematic review and meta-analysis of randomized controlled trials
- Review, Nor, NA
*MDA↓, *SOD↑, *IL6↓, *ROS↓, *Inflam↓,
5365- AV,    Aloe Vera Polysaccharides as Therapeutic Agents: Benefits Versus Side Effects in Biomedical Applications
- Review, Nor, NA - Review, IBD, NA - Review, Diabetic, NA
*Wound Healing↑, *Imm↑, *antiOx↑, *AntiDiabetic↑, *AntiCan↑, *Inflam↓, *NF-kB↓, *COX2↓, *5LO↓, *IL1β↓, *IL6↓, *TNF-α↓, *IL10↑, *other↓, *ROS↓, *SOD↑, *Catalase↑, *GPx↑, *lipid-P↓, *DNAdam↓, *GutMicro↑, *ZO-1↑, AntiTum↑, Casp3↑, Casp9↑, angioG↓, MMPs↓, VEGF↓, NK cell↑,
1530- Ba,    Baicalein Decreases Hydrogen Peroxide‐Induced Damage to NG108‐15 Cells via Upregulation of Nrf2
- in-vitro, Nor, NG108-15
*12LOX↓, *ROS↓, *NRF2↑, *eff↑,
1527- Ba,    Baicalein Alleviates Arsenic-induced Oxidative Stress through Activation of the Keap1/Nrf2 Signalling Pathway in Normal Human Liver Cells
- in-vitro, Nor, MIHA
*p‑NRF2↑, *ROS↓, *MDA↓, *antiOx↑,
1522- Ba,    Baicalein reduces lipopolysaccharide-induced inflammation via suppressing JAK/STATs activation and ROS production
- in-vitro, Nor, RAW264.7
*p‑STAT1↓, *p‑STAT3↓, *p‑JAK1↓, *p‑JAK2↓, *iNOS↓, *NO↓, *IL1β↓, *IL6↓, *TNF-α↓, *ROS↓,
2474- Ba,    Anticancer properties of baicalein: a review
- Review, Var, NA - in-vitro, Nor, BV2
ROS⇅, ROS↑, ER Stress↑, Ca+2↑, Apoptosis↑, eff↑, DR5↑, 12LOX↓, Cyt‑c↑, Casp7↑, Casp9↑, Casp3↑, cl‑PARP↑, TumCCA↑, cycE/CCNE↑, CDK4↓, cycD1/CCND1↓, VEGF↓, cMyc↓, Hif1a↓, NF-kB↓, BioEnh↑, BioEnh↑, P450↓, *Hif1a↓, *iNOS↓, *COX2↓, *VEGF↓, *ROS↓, *PI3K↓, *Akt↓,
2611- Ba,    Baicalein as a potent neuroprotective agent: A review
- Review, Nor, NA - Review, AD, NA - Review, Park, NA
*neuroP↑, *ROS↓, *β-Amyloid↓,
2624- Ba,    Baicalein inhibition of hydrogen peroxide-induced apoptosis via ROS-dependent heme oxygenase 1 gene expression
- in-vitro, Nor, RAW264.7
*HO-1↑, *ERK↑, *ROS↓, *eff↑, *MMP↑, *Cyt‑c∅,
2623- Ba,    Activation of the Nrf2/HO-1 signaling pathway contributes to the protective effects of baicalein against oxidative stress-induced DNA damage and apoptosis in HEI193 Schwann cells
- in-vitro, Nor, HEI193
*DNAdam↓, *ROS↓, *Bax:Bcl2↓, *p‑NRF2↑, *HO-1↑, *neuroP↑, *MMP↑,
2630- Ba,    Baicalein decreases uric acid and prevents hyperuricemic nephropathy in mice
- in-vivo, Nor, NA
*RenoP↑, *uricA↓, *ROS↓, EMT↓,
2613- Ba,    Hepatoprotective Effect of Baicalein Against Acetaminophen-Induced Acute Liver Injury in Mice
- in-vivo, Nor, NA
*hepatoP↑, *MDA↓, *SOD↑, *Catalase↑, *GSH↑, *MAPK↓, *p‑JAK2↓, *p‑STAT3↓, *ALAT↓, *AST↓, *ROS↓, *antiOx↑,
2294- Ba,    Baicalein attenuates cardiac hypertrophy in mice via suppressing oxidative stress and activating autophagy in cardiomyocytes
- in-vivo, Nor, NA
*Catalase↑, *ROS↓, *cardioP↑, *FOXO3?,
1380- BBR,  doxoR,    treatment with ROS scavenger N-acetylcysteine (NAC) and JNK inhibitor SP600125 could partially attenuate apoptosis and DNA damage triggered by DCZ0358.
- in-vivo, Nor, NA
*ROS↓, *MDA↓, *SOD↑, *NRF2↑, *HO-1↑,
2689- BBR,    Berberine protects against glutamate-induced oxidative stress and apoptosis in PC12 and N2a cells
- in-vitro, Nor, PC12 - in-vitro, AD, NA - in-vitro, Stroke, NA
*ROS↓, *lipid-P↓, *DNAdam↓, *GSH↑, *SOD↑, *eff↑, *cl‑Casp3↓, *BAX↓, *neuroP↑, *Dose↝, *Ca+2↓,
2676- BBR,    Berberine protects rat heart from ischemia/reperfusion injury via activating JAK2/STAT3 signaling and attenuating endoplasmic reticulum stress
- in-vivo, Nor, NA - in-vivo, CardioV, NA
*cardioP↑, *ROS↓, *ER Stress↓, *p‑PERK↓, *p‑eIF2α↓, *ATF4↓, CHOP↓, *JAK2↑, *STAT3↑, *UPR↓,
2724- BetA,    Down-regulation of NOX4 by betulinic acid protects against cerebral ischemia-reperfusion in mice
- in-vivo, Nor, NA - in-vivo, Stroke, NA
AntiTum↑, *Inflam↓, *ROS↓, *NOX4↓, *Apoptosis↓, neuroP↑,
2725- BetA,    Betulinic acid protects against renal damage by attenuation of oxidative stress and inflammation via Nrf2 signaling pathway in T-2 toxin-induced mice
- in-vivo, Nor, NA
*RenoP↑, *SOD?, *Catalase↑, *GSH↑, *ROS↓, *MDA↓, *IL1β↓, *TNF-α↓, *IL10↓, *IL6↑, *NRF2↑,
2758- BetA,    Betulinic Acid Attenuates Oxidative Stress in the Thymus Induced by Acute Exposure to T-2 Toxin via Regulation of the MAPK/Nrf2 Signaling Pathway
- in-vivo, Nor, NA
*ROS↓, *MDA↓, *SOD↑, *GSH↑, *p‑p38↓, *p‑JNK↓, *p‑ERK↓, *NRF2↑, *HO-1↑, *MAPK↓, *heparanase↑, *antiOx↑,
5669- BNL,    Comparison of pharmacological activity and safety of different stereochemical configurations of borneol: L-borneol, D-borneol, and synthetic borneol
- Review, Nor, NA - Review, AD, NA - Review, Stroke, NA
*eff↑, *eff↑, *toxicity↝, *Inflam↓, *Bacteria↓, *neuroP↑, *Half-Life↝, *BBB↑, *BioEnh↑, *P-gp↓, *CYP3A4↓, *ROS↓, *neuroP↑,
5671- BNL,    (+)-Borneol inhibits the generation of reactive oxygen species and neutrophil extracellular traps induced by phorbol-12-myristate-13-acetate
- in-vitro, Nor, NA
*ROS↓,
3510- Bor,    Boron Affects the Development of the Kidney Through Modulation of Apoptosis, Antioxidant Capacity, and Nrf2 Pathway in the African Ostrich Chicks
- in-vivo, Nor, NA
*RenoP↑, *ROS↓, *antiOx↑, *Apoptosis↓, *NRF2↑, *HO-1↑, *MDA↓, *lipid-P↓, *GPx↓, *Catalase↑, *SOD↑, *ALAT↓, *AST↓, *ALP↓,
731- Bor,    Protective Effect of Boric Acid Against Ochratoxin A-Induced Toxic Effects in Human Embryonal Kidney Cells (HEK293): A Study on Cytotoxic, Genotoxic, Oxidative, and Apoptotic Effects
- in-vitro, Nor, HEK293
*ROS↓,
2778- Bos,    Development, Analytical Characterization, and Bioactivity Evaluation of Boswellia serrata Extract-Layered Double Hydroxide Hybrid Composites
- in-vitro, Nor, NA
*ATP↓, *ROS↓,
1425- Bos,    Protective Effect of Boswellic Acids against Doxorubicin-Induced Hepatotoxicity: Impact on Nrf2/HO-1 Defense Pathway
- in-vivo, Nor, NA
*ChemoSen↑, *NRF2↑, *HO-1↑, *ROS↓, *lipid-P↓, *DNAdam↓,
5755- CA,    Caffeic Acid as a Promising Natural Feed Additive: Advancing Sustainable Aquaculture
- Review, Nor, NA
*Imm↑, *Inflam↓, *Bacteria↓, *eff↑, *ROS↓, *MDA↓, *Catalase↑, *GSH↑, *TAC↑, *NF-kB↓, *NLRP3↓, *eff↑, *AST↓, *ALAT↓, *SOD↑, *GSTA1↑,
5871- CA,    Carnosic Acid Attenuates an Early Increase in ROS Levels during Adipocyte Differentiation by Suppressing Translation of Nox4 and Inducing Translation of Antioxidant Enzymes
- in-vitro, Nor, NA
*ROS↓, *NF-kB↓, *Nrf1↑, *HO-1↑, *GSTs↑,
5873- CA,    Carnosic acid serves as a dual Nrf2 activator and PTEN/AKT suppressor to inhibit traumatic heterotopic ossification
- vitro+vivo, Nor, NA
*NRF2↑, *NOX↓, *TAC↑, *ROS↓, *NQO1↑, *p‑PTEN↑, RUNX2↓, SOX9↓,
5834- CAP,    Capsaicin and TRPV1: A Novel Therapeutic Approach to Mitigate Vascular Aging
- Study, Nor, NA
*AntiCan↑, *Inflam↓, *antiOx↑, *TRPV1↑, *AMPK↑, *SIRT1↑, *NADPH↓, *ROS↓, *MAPK↓, *eNOS↑, *Wnt/(β-catenin)↓, RenoP↑,
5830- CAP,    Inhibition of pyroptosis and apoptosis by capsaicin protects against LPS-induced acute kidney injury through TRPV1/UCP2 axis in vitro
- in-vitro, Nor, HK-2
*IL1β↓, *IL18↓, *TRPV1↑, *ROS↓, *MMP↑, *Apoptosis↓, *RenoP↑, *Inflam↓, *UCPs↑,
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↓,
2394- CAP,    Capsaicin acts as a novel NRF2 agonist to suppress ethanol induced gastric mucosa oxidative damage by directly disrupting the KEAP1-NRF2 interaction
- in-vitro, Nor, GES-1
*mtDam↓, *NRF2↑, *HO-1↑, *Trx↑, *GSS↑, *NQO1↑, *Keap1↓, *ROS↓, *PKM2↓, *LDHA↓, *Inflam↓,
2348- CAP,    Recent advances in analysis of capsaicin and its effects on metabolic pathways by mass spectrometry
- Analysis, Nor, NA
Warburg↓, *PKM2↓, *COX2↓, *Inflam↓, *Sepsis↓, *AMPK↑, *PKA↑, *mitResp↑, *FAO↑, *FASN↓, *PGM1?, *ATP↑, *ROS↓,
5902- CAR,    A novel antagonist of TRPM2 and TRPV4 channels: Carvacrol
- in-vitro, Nor, HEK293
*other↓, *GSH↑, *GPx↑, *ROS↓, *Apoptosis↓,
6022- CGA,    Chlorogenic Acid: Recent Advances on Its Dual Role as a Food Additive and a Nutraceutical against Metabolic Syndrome
- Review, Nor, NA
*antiOx↑, *Inflam↓, *AntiDiabetic↑, *Obesity↓, *Wound Healing↑, *BP↓, *Dose↝, *ROS↓, *Fas↓, *HMG-CoA↓, *GutMicro↑,
6010- CGA,    The Biological Activity Mechanism of Chlorogenic Acid and Its Applications in Food Industry: A Review
- Review, Nor, NA
*antiOx↑, *hepatoP↑, *RenoP↑, AntiTum↑, *glucose↝, *Inflam↓, *neuroP↑, *ROS↓, *Keap1↓, *NRF2↑, *SOD↑, *Catalase↑, *GPx↑, *GSH↑, *MDA↓, *p‑ERK↑, *GRP78/BiP↑, *CHOP↑, *GRP94↑, *Casp3↓, *Casp9↓, *HGF/c-Met↑, *TNF-α↓, *TLR4↓, *MAPK↓, *IL1β↓, *iNOS↓, TCA↓, Glycolysis↓, Bcl-2↓, BAX↑, MAPK↑, JNK↑, CSCs↓, Nanog↓, SOX2↓, CD44↓, OCT4↓, P53↑, P21↑, *SOD1↑, *AGEs↓, *GLUT2↑, *HDL↑, *Fas↓, *HMG-CoA↓, *NF-kB↓, *HO-1↓, *COX2↓, *TLR4↓, *BioAv↑, *BioAv↝, TumCP↓, TumCMig↓, TumCI↓,

Showing Research Papers: 1 to 50 of 204
Page 1 of 5 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 204

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↓, 1,   Keap1↓, 1,   NADH↓, 1,   ROS↑, 3,   ROS⇅, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   MPT↑, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   cMyc↓, 1,   Glycolysis↓, 1,   SIRT1↓, 1,   TCA↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   BAX↑, 1,   BAX⇅, 1,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 2,   Casp7↑, 1,   Casp9↑, 2,   Cyt‑c↑, 2,   DR5↑, 1,   JNK↑, 1,   MAPK↑, 1,   p38↑, 1,  

Kinase & Signal Transduction ⓘ

SOX9↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   ER Stress↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↑, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   CSCs↓, 1,   EMT↓, 1,   Nanog↓, 1,   OCT4↓, 1,   RUNX2↓, 1,   SOX2↓, 1,   TOP1↓, 1,   TOP2↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 1,   MMPs↓, 1,   TRIB3↑, 1,   TumCI↓, 1,   TumCMig↓, 3,   TumCP↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,   NK cell↑, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 2,   ChemoSen↑, 1,   eff↑, 1,   P450↓, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

TRIB3↑, 1,  

Functional Outcomes ⓘ

AntiTum↑, 3,   chemoP↑, 1,   neuroP↑, 2,   Obesity↓, 1,   radioP↑, 1,   RenoP↑, 1,  
Total Targets: 70

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 11,   Catalase↓, 1,   Catalase↑, 9,   Ferroptosis↓, 1,   GPx↓, 1,   GPx↑, 5,   GSH↑, 10,   GSS↑, 1,   GSTA1↑, 1,   GSTs↑, 1,   HDL↑, 1,   HO-1↓, 1,   HO-1↑, 10,   Keap1↓, 2,   lipid-P↓, 4,   MDA↓, 13,   MPO↓, 1,   NOX4↓, 2,   NQO1↑, 2,   Nrf1↑, 1,   NRF2↑, 13,   p‑NRF2↑, 2,   ROS↓, 50,   ROS↑, 1,   SOD?, 1,   SOD↑, 10,   SOD1↑, 2,   SOD2↑, 1,   TAC↑, 3,   Trx↑, 1,   UCPs↑, 1,   uricA↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ATP↑, 1,   mitResp↑, 1,   MMP↑, 3,   mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   ALAT↓, 5,   AMPK↑, 3,   CYP3A4↓, 1,   FAO↑, 1,   FASN↓, 1,   glucose↝, 1,   GLUT2↑, 1,   HMG-CoA↓, 2,   LDH↓, 1,   LDHA↓, 1,   NADPH↓, 1,   PGM1?, 1,   PKM2↓, 4,   SIRT1↑, 2,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↓, 4,   BAX↓, 1,   Bax:Bcl2↓, 1,   Casp3↓, 1,   cl‑Casp3↓, 1,   Casp9↓, 1,   Cyt‑c∅, 1,   Fas↓, 2,   Ferroptosis↓, 1,   HGF/c-Met↑, 1,   iNOS↓, 4,   p‑JNK↓, 1,   MAPK↓, 4,   p‑p38↓, 2,   TRPV1↑, 3,  

Transcription & Epigenetics ⓘ

other↓, 2,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   p‑eIF2α↓, 1,   ER Stress↓, 1,   GRP78/BiP↑, 1,   GRP94↑, 1,   p‑PERK↓, 1,   UPR↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 4,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   p‑ERK↓, 2,   p‑ERK↑, 1,   FOXO3?, 1,   PI3K↓, 2,   p‑PTEN↑, 1,   p‑STAT1↓, 1,   STAT3↑, 1,   p‑STAT3↓, 2,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

5LO↓, 1,   Ca+2↓, 1,   Ca+2↑, 1,   COL3A1↓, 1,   heparanase↑, 1,   PKA↑, 1,   PKCδ↑, 1,   TGF-β↓, 1,   VCAM-1↓, 1,   Vim↓, 1,   ZO-1↑, 1,   α-SMA↓, 2,  

Angiogenesis & Vasculature ⓘ

ATF4↓, 1,   eNOS↑, 1,   Hif1a↓, 3,   NO↓, 2,   VEGF↓, 2,  

Barriers & Transport ⓘ

BBB↓, 1,   BBB↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 5,   ICAM-1↓, 1,   IFN-γ↓, 1,   IL1↓, 1,   IL10↓, 1,   IL10↑, 2,   IL18↓, 1,   IL1β↓, 6,   IL4↑, 1,   IL5↑, 1,   IL6↓, 6,   IL6↑, 1,   Imm↑, 2,   Inflam↓, 17,   p‑JAK1↓, 1,   JAK2↑, 1,   p‑JAK2↓, 2,   NF-kB↓, 11,   TLR4↓, 3,   TNF-α↓, 7,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,  

Protein Aggregation ⓘ

AGEs↓, 1,   Aβ↓, 1,   NLRP3↓, 3,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 2,   BioEnh↑, 1,   ChemoSen↑, 1,   Dose↝, 4,   eff↑, 8,   Half-Life↓, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 5,   ALP↓, 2,   AST↓, 5,   BP↓, 1,   GutMicro↑, 3,   IL6↓, 6,   IL6↑, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 3,   AntiDiabetic↑, 2,   cardioP↑, 5,   hepatoP↑, 5,   neuroP↑, 7,   Obesity↓, 1,   RenoP↑, 5,   toxicity↓, 3,   toxicity↝, 1,   Wound Healing↑, 2,  

Infection & Microbiome ⓘ

Bacteria↓, 2,   Sepsis↓, 1,  
Total Targets: 163

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
15 Thymoquinone
12 Quercetin
10 Baicalein
9 Honokiol
9 Radiotherapy/Radiation
9 Magnetic Fields
8 Resveratrol
8 doxorubicin
8 Propolis -bee glue
7 Vitamin C (Ascorbic Acid)
7 Selenium NanoParticles
7 Sulforaphane (mainly Broccoli)
7 Shikonin
6 Chlorogenic acid
6 Luteolin
5 Silver-NanoParticles
5 Capsaicin
5 EGCG (Epigallocatechin Gallate)
5 Lycopene
5 Rosmarinic acid
5 Silymarin (Milk Thistle) silibinin
5 Vitamin K2
4 Curcumin
3 Selenite (Sodium)
3 Alpha-Lipoic-Acid
3 Berberine
3 Betulinic acid
3 diet Methionine-Restricted Diet
3 Fisetin
3 HydroxyCitric Acid
3 nicotinamide adenine dinucleotide
3 Phenylbutyrate
2 Cisplatin
2 Apigenin (mainly Parsley)
2 Artemisinin
2 Astaxanthin
2 borneol
2 Boron
2 Boswellia (frankincense)
2 Carnosic acid
2 Chlorophyllin
2 Magnetic Field Rotating
2 Urolithin
1 Allicin (mainly Garlic)
1 Andrographis
1 Aloe anthraquinones
1 Caffeic acid
1 Carvacrol
1 Chocolate
1 Choline
1 Coenzyme Q10
1 Electrical Pulses
1 Fucoidan
1 γ-linolenic acid (Borage Oil)
1 Graviola
1 Hydrogen Gas
1 Huperzine A/Huperzia serrata
1 Juglone
1 Chrysin
1 Metformin
1 Piperine
1 Piperlongumine
1 Pterostilbene
1 Rutin
1 Selenium
1 Gold NanoParticles
1 chitosan
1 acetaminophen
1 Salvia miltiorrhiza
1 Aflavin-3,3′-digallate
1 5-fluorouracil
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:49  Cells:%  prod#:%  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page