Curcumin / NRF2 Cancer Research Results

CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of NRF2↑">Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown
-may suppress CSC: suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).
Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
curcumin can act as a pro-oxidant when blue light is applied
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑">NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑">NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Driver Suppression of survival and inflammatory transcription NF-κB is a primary, repeatedly validated curcumin target explaining pleiotropic downstream effects
2 STAT3 signaling ↓ STAT3 phosphorylation / activity ↔ or mild suppression Driver Loss of pro-survival and proliferative signaling STAT3 inhibition contributes to growth arrest, apoptosis sensitization, and reduced cytokine signaling in tumors
3 Reactive oxygen species (ROS) ↑ ROS (dose- & context-dependent) ↓ ROS / buffered Conditional Driver Biphasic redox modulation Curcumin can act as a pro-oxidant in cancer cells with high basal stress while acting antioxidant in normal cells
4 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Driver Execution of intrinsic apoptosis Mitochondrial dysfunction and caspase activation occur downstream of NF-κB/STAT3 and ROS effects
5 PI3K → AKT → mTOR axis ↓ AKT / ↓ mTOR ↔ or adaptive suppression Secondary Reduced growth and anabolic signaling AKT/mTOR inhibition contributes to growth suppression and autophagy induction in cancer cells
6 Autophagy ↑ autophagy (protective or pro-death) ↑ adaptive autophagy Secondary Stress adaptation vs cell death Autophagy may be cytoprotective or cooperate with apoptosis depending on context and dose
7 HIF-1α / VEGF hypoxia–angiogenesis axis ↓ HIF-1α; ↓ VEGF ↔ minimal effect Secondary Anti-angiogenic pressure Suppression of hypoxia-driven transcription limits angiogenesis and tumor adaptation
8 Cell cycle regulation ↑ G2/M or G1 arrest ↔ largely spared Phenotypic Cytostatic growth control Cell-cycle arrest reflects upstream signaling and epigenetic effects rather than direct CDK inhibition
9 Migration / invasion (EMT, MMP axis) ↓ migration & invasion ↔ Phenotypic Anti-metastatic phenotype Reduced EMT markers and protease activity limit invasive behavior
10 Epigenetic regulation (p300/CBP HAT activity) ↓ histone acetylation ↔ modest Secondary Transcriptional reprogramming Curcumin modulates chromatin via HAT inhibition rather than classic HDAC inhibition


NRF2, nuclear factor erythroid 2-related factor 2: Click to Expand ⟱
Source: TCGA
Type: Antiapoptotic
Nrf2 is responsible for regulating an extensive panel of antioxidant enzymes involved in the detoxification and elimination of oxidative stress. Thought of as "Master Regulator" of antioxidant response.
-One way to estimate Nrf2 induction is through the expression of NQO1.
NQO1, the most potent inducer:
SFN 0.2 μM,
quercetin (2.5 μM),
curcumin (2.7 μM),
Silymarin (3.6 μM),
tamoxifen (5.9 μM),
genistein (6.2 μM ),
beta-carotene (7.2μM),
lutein (17 μM),
resveratrol (21 μM),
indol-3-carbinol (50 μM),
chlorophyll (250 μM),
alpha-cryptoxanthin (1.8 mM),
and zeaxanthin (2.2 mM)

1. Raising Nrf2 enhances the cell's antioxidant defenses and ↓ROS. This strategy is used to decrease chemo-radio side effects.
2. Downregulating Nrf2 lowers antioxidant defenses and ↑ROS. In cancer cells this leads to DNA damage, and cell death.
3. However there are some cases where increasing Nrf2 paradoxically causes an increase in ROS (cancer cells). Such as cases of Mitochondial overload, signal crosstalk, reductive stress

-In some cases, Nrf2 is overexpressed in cancer cells, which can lead to the activation of genes involved in cell proliferation, angiogenesis, and metastasis. This can contribute to the development of resistance to chemotherapy and targeted therapies.
-Increased Nrf2 expression: Lung, Breast, Colorectal, Prostrate.
Decreased Nrf2 expression: Skine, Liver, Pancreatic.
-Nrf2 is a cytoprotective transcription factor which demonstrated both a negative effect as well as a positive effect on cancer
- "promotes Nrf2 translocation from the cytoplasm to the nucleus," means facilitates the movement of Nrf2 into the nucleus, thereby enhancing the cell's antioxidant and cytoprotective responses. -Major regulator of Nrf2 activity in cells is the cytosolic inhibitor Keap1.

Nrf2 Inhibitors and Activators
Nrf2 Inhibitors: Brusatol, Luteolin, Trigonelline, VitC, Retinoic acid, Chrysin
Nrf2 Activators: SFN, OPZ EGCG, Resveratrol, DATS, CUR, CDDO, Api
- potent Nrf2 inducers from plants include sulforaphane, curcumin, EGCG, resveratrol, caffeic acid phenethyl ester, wasabi, cafestol and kahweol (coffee), cinnamon, ginger, garlic, lycopene, rosemany

Nrf2 plays dual roles in that it can protect normal tissues against oxidative damage and can act as an oncogenic protein in tumor tissue.
– In healthy tissues, NRF2 activation helps protect cells from oxidative damage and maintains cellular homeostasis.
– In many cancers, constitutive activation of NRF2 (often through mutations in NRF2 itself or loss-of-function mutations in KEAP1) leads to an enhanced antioxidant capacity.
– This upregulation can promote tumor cell survival by enabling cancer cells to thrive under oxidative stress, resist chemotherapeutic agents, and sustain metabolic reprogramming.
– Elevated NRF2 levels have been implicated in promoting tumor growth, metastasis, and resistance to therapy in various malignancies.
– High or sustained NRF2 activity is frequently associated with aggressive tumor phenotypes, poorer prognosis, and decreased overall survival in several cancer types.
– While its activation is essential for protecting normal cells from oxidative stress, aberrant or sustained NRF2 activation in tumor cells can lead to enhanced survival, therapeutic resistance, and tumor progression.

NRF2 inhibitors: (to decrease antioxidant defenses and increase cell death from ROS).
-Brusatol: most cited natural inhibitors of Nrf2.
-Luteolin: luteolin can reduce Nrf2 activity in specific cancer models and may enhance cell sensitivity to chemotherapy. However, luteolin is also known as an antioxidant, and its influence on Nrf2 can sometimes be context dependent.
-Apigenin: certain studies to down‑regulate Nrf2 in cancer cells: Dose and context dependent .
-Oridonin:
-Wogonin: although its effects might be cell‑ and dose‑specific.
- Withaferin A

Scientific Papers found: Click to Expand⟱
3795- CUR,    Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence
- Review, AD, NA
*antiOx↑, *Inflam↓, *AntiAge↑, *AMPK↑, *SIRT1↑, *NF-kB↓, *mTOR↓, *NLRP3↓, *NADPH↓, *ROS↓, *COX2↓, *MCP1↓, *IL1β↓, *IL17↓, *IL23↓, *TNF-α↓, *MPO↓, *IL10↑, *lipid-P↓, *SOD↑, *Aβ↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓, *TXNIP↓, *NRF2↑, *NQO1↑, *HO-1↑, *OS↑, *memory↑, *BDNF↑, *neuroP↑, *BACE↓, *AChE↓, *LDL↓,
3794- CUR,    Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities
- Review, AD, NA
*GSK‐3β↓, *CDK5↓, *p‑tau↓, *IronCh↑, *ROS↓, *HO-1↑, *SOD↑, *Catalase↑, *GSH↑, *TNF-α↓, *IL6↓, *IL12↓, *NRF2↑, *PPARγ↑, *IL4↑, *AChE↓, *Dose↝, *GutMicro↑,
4881- CUR,  SFN,  RES,  EGCG,  Lyco  An update of Nrf2 activators and inhibitors in cancer prevention/promotion
- Review, Var, NA
*NRF2↑, *antiOx↑,
4831- CUR,    The dual role of curcumin and ferulic acid in counteracting chemoresistance and cisplatin-induced ototoxicity
- in-vitro, NA, NA
*NRF2↑, *P53↓, *NF-kB↓, ROS↑, Inflam↓, ChemoSen↑,
2821- CUR,    Antioxidant curcumin induces oxidative stress to kill tumor cells (Review)
- Review, Var, NA
*antiOx↑, *NRF2↑, *ROS↓, *Inflam↓, ROS↑, p‑ERK↑, ER Stress↑, mtDam↑, Apoptosis↑, Akt↓, mTOR↓, HO-1↑, Fenton↑, GSH↓, Iron↑, p‑JNK↑, Cyt‑c↑, ATF6↑, CHOP↑,
2819- CUR,  Chemo,    Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury
- Review, Var, NA
*hepatoP↑, *Inflam↓, *antiOx↑, *lipid-P↓, *GSH↑, *SOD↑, *Catalase↑, *GPx↑, *GSTs↑, *ROS↓, *ALAT↓, *AST↓, *MDA↓, *NRF2↑, *COX2↑, *NF-kB↓, *ICAM-1↓, *MCP1↓, *HO-1↑, CXCc↓,
2818- CUR,    Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways
- Review, AD, NA
*neuroP↑, *ROS↓, *Inflam↓, *Apoptosis↓, *cognitive↑, *cardioP↑, other↑, *COX2↓, *IL1β↓, *TNF-α↓, NF-kB↓, *PGE2↓, *iNOS↓, *NO↓, *IL2↓, *IL4↓, *IL6↓, *INF-γ↓, *GSK‐3β↓, *STAT↓, *GSH↑, *MDA↓, *lipid-P↓, *SOD↑, *GPx↑, *Catalase↑, *GSR↓, *LDH↓, *H2O2↓, *Casp3↓, *Casp9↓, *NRF2↑, *AIF↓, *ATP↑,
3581- CUR,    Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer's Disease
- NA, AD, NA
*antiOx↑, *Inflam↓, *BBB↑, *NRF2↑, *NF-kB↓, *cognitive↑, *ROS↓, *MDA↓, *SOD↑, *Catalase↑, *INF-γ↓, *IL4↓, *memory↑, *TNF-α↓, *IL1β↓,
3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, *antiOx↑, *memory↑, *Aβ↓, *BBB↑, *cognitive↑, *tau↓, *LDL↓, *AChE↓, *IL1β↓, *IronCh↑, *neuroP↑, *BioAv↝, *PI3K↑, *Akt↑, *NRF2↑, *HO-1↑, *Ferritin↑, *HO-2↓, *ROS↓, *Ach↑, *GSH↑, *Bcl-2↑, *ChAT↑,
1485- CUR,  Chemo,  Rad,    Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs
- Review, Var, NA
ChemoSen↑, NF-kB↓, *STAT3↓, *COX2↓, *Akt↓, *NRF2↑, *HO-1↑, *GPx↑, *NADPH↑, *GSH↑, *ROS↓, *p300↓, radioP↑, chemoP↑, RadioS↑,
1510- CUR,  Chemo,    Combination therapy in combating cancer
- Review, NA, NA
*NRF2↑, *GSH↑, *ROS↓, ChemoSideEff↓, eff↑, OS↓, chemoP↑,
13- CUR,    Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
- Review, BC, NA
P53↑, DR5↑, JNK↑, NRF2↑, PPARγ↑, HER2/EBBR2↓, IR↓, ER(estro)↓, Fas↑, PDGF↓, TGF-β↓, FGF↓, EGFR↓, JAK↓, PAK↓, MAPK↓, ATPase↓, COX2↓, MMPs↓, IL1↓, IL2↓, IL5↓, IL6↓, IL8↓, IL12↓, IL18↓, NF-kB↓, NOTCH1↓, STAT1↓, STAT4↓, STAT5↓, STAT3↓,
414- CUR,    Transcriptome Investigation and In Vitro Verification of Curcumin-Induced HO-1 as a Feature of Ferroptosis in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Ferroptosis↑, Iron↑, ROS↑, lipid-P↑, MDA↑, GSH↓, HO-1↑, NRF2↑, GPx↓, ROS↑, Iron↑, GPx4↓, HSP70/HSPA5↑, ATFs↑, CHOP↑, MDA↑, FTL↑, FTH1↑, BACH1↑, REL↑, USF1↑, NFE2L2↑,
405- CUR,  5-FU,    Curcumin activates a ROS/KEAP1/NRF2/miR-34a/b/c cascade to suppress colorectal cancer metastasis
- vitro+vivo, CRC, HCT116
Apoptosis↑, TumCMig↓, NRF2↑, ROS↑, MET↑, miR-34a↑,
410- CUR,    Nrf2 depletion enhanced curcumin therapy effect in gastric cancer by inducing the excessive accumulation of ROS
- vitro+vivo, GC, AGS - vitro+vivo, GC, HGC27
ROS↑, NRF2↑,
4827- QC,  CUR,    Synthetic Pathways and the Therapeutic Potential of Quercetin and Curcumin
- Review, Var, NA
*AntiCan↑, *Inflam↓, *Bacteria↓, *AntiDiabetic↑, *ROS↓, *SOD↑, *Catalase↑, *GSH↑, *NRF2↑, *Trx↑, *IronCh↑, *MDA↑, cycD1/CCND1↓, PI3K↓, Casp3↑, BAX↑, ChemoSen↑, ROS↑, eff↑, MMP↓, Cyt‑c↑, Akt↓, ERK↓,
2133- TQ,  CUR,  Cisplatin,    Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling
- in-vitro, Nor, HEK293 - in-vivo, NA, NA
*creat↓, *TNF-α↓, *IL6↓, *MRP↓, *GFR↑, *mt-ATPase↑, *p‑Akt↑, *NRF2↑, *HO-1↑, *Casp3↓, *NF-kB↓, *RenoP↑,

Showing Research Papers: 1 to 17 of 17

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Fenton↑, 1,   Ferroptosis↑, 1,   GPx↓, 1,   GPx4↓, 1,   GSH↓, 2,   HO-1↑, 2,   Iron↑, 3,   lipid-P↑, 1,   MDA↑, 2,   NFE2L2↑, 1,   NRF2↑, 4,   ROS↑, 7,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,   FTL↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

IR↓, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Casp3↑, 1,   Cyt‑c↑, 2,   DR5↑, 1,   Fas↑, 1,   Ferroptosis↑, 1,   JNK↑, 1,   p‑JNK↑, 1,   MAPK↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   PAK↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,   USF1↑, 1,  

Protein Folding & ER Stress ⓘ

ATF6↑, 1,   ATFs↑, 1,   CHOP↑, 2,   ER Stress↑, 1,   HSP70/HSPA5↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   p‑ERK↑, 1,   FGF↓, 1,   miR-34a↑, 1,   mTOR↓, 1,   NOTCH1↓, 1,   PI3K↓, 1,   STAT1↓, 1,   STAT3↓, 1,   STAT4↓, 1,   STAT5↓, 1,  

Migration ⓘ

ATPase↓, 1,   BACH1↑, 1,   MET↑, 1,   MMPs↓, 1,   PDGF↓, 1,   TGF-β↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,   REL↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCc↓, 1,   IL1↓, 1,   IL12↓, 1,   IL18↓, 1,   IL2↓, 1,   IL5↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 1,   JAK↓, 1,   NF-kB↓, 3,  

Hormonal & Nuclear Receptors ⓘ

ER(estro)↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   eff↑, 2,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 2,   ChemoSideEff↓, 1,   OS↓, 1,   radioP↑, 1,  
Total Targets: 83

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 6,   Catalase↑, 5,   GPx↑, 3,   GSH↑, 7,   GSR↓, 1,   GSTs↑, 1,   H2O2↓, 1,   HO-1↑, 6,   HO-2↓, 1,   lipid-P↓, 3,   MDA↓, 3,   MDA↑, 1,   MPO↓, 1,   NQO1↑, 1,   NRF2↑, 13,   ROS↓, 10,   SOD↑, 6,   Trx↑, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↑, 1,   IronCh↑, 3,  

Mitochondria & Bioenergetics ⓘ

AIF↓, 1,   ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 1,   LDH↓, 1,   LDL↓, 2,   NADPH↓, 1,   NADPH↑, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   p‑Akt↑, 1,   Apoptosis↓, 1,   Bcl-2↑, 1,   Casp3↓, 2,   Casp9↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 3,   mTOR↓, 1,   p300↓, 1,   PI3K↑, 1,   STAT↓, 1,   STAT3↓, 1,  

Migration ⓘ

mt-ATPase↑, 1,   CDK5↓, 2,   TXNIP↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,   MRP↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   COX2↑, 1,   ICAM-1↓, 1,   IL10↑, 1,   IL12↓, 1,   IL17↓, 1,   IL1β↓, 4,   IL2↓, 1,   IL23↓, 1,   IL4↓, 2,   IL4↑, 1,   IL6↓, 3,   INF-γ↓, 2,   Inflam↓, 7,   MCP1↓, 2,   NF-kB↓, 5,   PGE2↓, 1,   TNF-α↓, 5,  

Synaptic & Neurotransmission ⓘ

AChE↓, 3,   BDNF↑, 1,   ChAT↑, 1,   tau↓, 1,   p‑tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   Dose↝, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   creat↓, 1,   Ferritin↑, 1,   GutMicro↑, 1,   IL6↓, 3,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 1,   cognitive↑, 3,   GFR↑, 1,   hepatoP↑, 1,   memory↑, 3,   neuroP↑, 3,   OS↑, 1,   RenoP↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 99

Scientific Paper Hit Count for: NRF2, nuclear factor erythroid 2-related factor 2
17 Curcumin
3 Chemotherapy
1 Sulforaphane (mainly Broccoli)
1 Resveratrol
1 EGCG (Epigallocatechin Gallate)
1 Lycopene
1 Radiotherapy/Radiation
1 5-fluorouracil
1 Quercetin
1 Thymoquinone
1 Cisplatin
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#:65  Target#:226  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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