Curcumin / ROS Cancer Research Results

CUR, Curcumin: Click to Expand ⟱

Features:

Curcumin is the main active ingredient in Turmeric. 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, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown
-may suppress CSC: suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).

Curcumin — Curcumin is a turmeric-derived polyphenolic curcuminoid and diarylheptanoid from Curcuma longa, functionally best classified as a natural-product small molecule / nutraceutical candidate with pleiotropic redox, inflammatory, transcriptional, metabolic, and chemosensitizing activity. The standard abbreviation is CUR. It is the principal active pigment of turmeric rhizome, usually studied as purified curcumin, curcuminoid mixtures, turmeric extract, phytosomal curcumin, liposomal curcumin, nanoparticle curcumin, or piperine-enhanced formulations. Its oncology relevance is mechanistically broad but clinically constrained by poor aqueous solubility, rapid metabolism, low free systemic exposure, formulation variability, and insufficient well-powered cancer outcome trials.

Primary mechanisms (ranked):

Suppression of NF-κB / STAT3 inflammatory-survival signaling, reducing cytokine, COX-2, iNOS, anti-apoptotic, invasion, and treatment-resistance programs.
Biphasic redox modulation: ROS buffering in normal/inflamed tissue but ROS↑, GSH depletion, thioredoxin reductase disruption, and oxidative stress amplification in susceptible cancer models at sufficient exposure.
Mitochondrial injury and intrinsic apoptosis, including mitochondrial membrane potential loss, cytochrome-c release, caspase activation, PARP cleavage, and ER-stress/UPR involvement.
PI3K/AKT/mTOR and MAPK pathway modulation, contributing to growth arrest, autophagy modulation, apoptosis sensitization, and reduced survival signaling.
Wnt/β-catenin, Hedgehog/GLI, Notch, and cancer-stem-cell suppression, reducing stemness, EMT, invasion, and recurrence-associated phenotypes in models.
Hypoxia / HIF-1α and glycolysis inhibition, including reduced GLUT1, HK2, LDHA, PKM2, lactate/ECAR, and Warburg-like metabolic support in selected models.
Anti-angiogenic and anti-metastatic modulation, including VEGF, MMPs, uPA, CXCR4/SDF-1, TGF-β/α-SMA, FAK, and EMT-related axes.
Epigenetic and transcriptional reprogramming, including reported HDAC, DNMT, EZH2, Sp-family, p53, and microRNA-related effects.
NRF2 modulation: generally cytoprotective in normal cells but potentially protective for cancer cells when NRF2 is activated; NRF2 suppression/knockdown can increase curcumin-induced ROS stress in some tumor models.
Chemosensitization and radiosensitization, with parallel normal-tissue protective signals reported in some mucositis, dermatitis, oxidative-stress, and radioprotection contexts.

Bioavailability / PK relevance: Conventional oral curcumin has poor systemic bioavailability because of low solubility, low absorption, rapid conjugation, and rapid elimination. Oral trials have used doses up to gram-level daily dosing, but circulating free curcumin is typically low; measured plasma exposure often reflects conjugated curcumin. Piperine, phospholipid/phytosome, micellar, liposomal, nanoparticle, and other enhanced formulations can raise exposure, but each formulation should be treated as a distinct translational entity. Delivery constraints are central for oncology interpretation.

In-vitro vs systemic exposure relevance: Common in-vitro anticancer concentrations, often in the low-to-mid micromolar range and sometimes higher, frequently exceed achievable free plasma exposure from standard oral curcumin. Therefore, direct systemic anticancer claims from cell culture should be weighted cautiously unless supported by tissue-local exposure, enhanced formulation data, local delivery, IV/liposomal delivery, or clinically measured pharmacodynamic biomarkers.

Clinical evidence status: Preclinical evidence is extensive; human oncology evidence is mainly small human, biomarker, pilot, chemoprevention, adjunctive, symptom-management, and formulation trials. Current authoritative oncology summaries judge evidence inadequate to recommend curcumin-containing products as cancer treatment or as routine adjunct anticancer therapy, although symptom-support areas such as oral mucositis, radiation dermatitis, oxidative-status measures, and quality of life have more suggestive but still confirmatory-level evidence.

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↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓">ROS↓, 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

Curcumin Cancer Mechanism Ranking

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	NF-κB / STAT3 inflammatory survival signaling	NF-κB ↓; STAT3 ↓; IL-6/TNF-α/COX-2/iNOS ↓; Bcl-2/Bcl-xL/survivin programs ↓	Inflammatory tone ↓; tissue-protective anti-inflammatory effect likely context-dependent	R/G	Reduced survival, inflammation, invasion, and therapy-resistance signaling	Most central and industry-relevant axis; explains many downstream effects but is not curcumin-specific.
2	Biphasic redox stress and antioxidant buffering	ROS ↑ (dose-dependent); GSH ↓; antioxidant reserve ↓; oxidative apoptosis ↑	ROS ↓; NRF2/SOD/GSH/catalase/HO-1 often ↑ in stress models	R/G	Selective redox pressure in susceptible tumor cells with normal-cell protection in lower-stress settings	Direction depends strongly on concentration, formulation, light exposure, basal redox state, and tumor antioxidant capacity.
3	Thioredoxin reductase and GSH linked redox systems	TrxR inhibition or redox cycling ↑; GSH depletion ↑; oxidative stress ↑	Usually buffered or antioxidant response ↑ at non-toxic exposure	R/G	Collapse of tumor redox compensation	Mechanistically important for ROS amplification and radiosensitization; achievable exposure remains a major constraint.
4	Mitochondrial depolarization and intrinsic apoptosis	ΔΨm ↓; cytochrome-c ↑; caspase-3/9 ↑; PARP cleavage ↑; apoptosis ↑	Generally ↔ or protected under oxidative/inflammatory stress	R/G	Execution of apoptosis after upstream redox and survival-signal disruption	Central cytotoxic endpoint in many cell models; often downstream of ROS, ER stress, AKT/mTOR suppression, or p53 modulation.
5	PI3K / AKT / mTOR and autophagy balance	PI3K ↓; AKT ↓; mTOR ↓; survival signaling ↓; autophagy ↑ or mixed	Stress-adaptive autophagy ↔ or ↑ (context-dependent)	R/G	Growth suppression and apoptosis sensitization	Autophagy may be cytotoxic or protective depending on model and timing; combination logic may require autophagy-state interpretation.
6	Wnt / β-catenin / Hedgehog / Notch stemness signaling	β-catenin ↓; GLI/Hedgehog ↓; Notch ↓; CD133/CD44/OCT4/SOX2-like stemness markers ↓	Generally ↔; possible normal stem-cell effects are tissue/context-dependent	G	Reduced cancer stemness, EMT, self-renewal, and recurrence-associated phenotypes	Important for anti-metastatic and anti-CSC positioning; evidence is mainly preclinical.
7	HIF-1α / glycolysis / Warburg metabolism	HIF-1α ↓; GLUT1 ↓; HK2 ↓; LDHA ↓; PKM2 ↓; lactate/ECAR ↓; ATP stress ↑	Metabolic effects ↔ or adaptive; normal-cell toxicity depends on exposure	G	Reduced hypoxic adaptation and glycolytic energy support	Mechanistically relevant but formulation and tissue exposure are critical; hypoxic tumors may be more relevant than normoxic cell culture.
8	EMT / invasion / metastasis matrix axis	EMT ↓; MMP2/MMP9 ↓; uPA ↓; FAK ↓; CXCR4/SDF-1 ↓; migration/invasion ↓	Inflammation-linked remodeling ↓; wound-healing effects context-dependent	G	Anti-invasive and anti-metastatic phenotype	Strongly supported in models; clinical anti-metastatic efficacy is not established.
9	VEGF / angiogenesis / hypoxia interface	VEGF ↓; HIF-1α ↓; angiogenic signaling ↓	Angiogenesis modulation ↔ or ↓ (context-dependent)	G	Reduced tumor vascular-support signaling	Overlaps with NF-κB, HIF-1α, STAT3, and inflammatory cytokine suppression.
10	Epigenetic and transcriptional reprogramming	HDAC ↓; DNMT1/3A ↓; EZH2 ↓; Sp proteins ↓; p53 ↑ or restored in selected models	Broad transcriptional effects possible; selectivity uncertain	G	Reactivation of growth-control and differentiation-associated programs	Biologically plausible but highly model-dependent; direct target specificity is lower than pathway-level interpretation.
11	Ferroptosis and iron redox stress	Iron/redox stress ↑; lipid peroxidation ↑; GPX4/GSH axis may ↓ (model-dependent)	Iron-chelation and antioxidant protection may occur (context-dependent)	R/G	Potential ferroptosis contribution in susceptible tumor models	Curcumin can behave as an iron chelator, antioxidant, or pro-oxidant depending on exposure, formulation, and cancer redox context.
12	NRF2 cytoprotection risk	NRF2 ↑ may protect tumor cells; NRF2 depletion can enhance curcumin-induced ROS stress in some models	NRF2 ↑ supports antioxidant and anti-inflammatory tissue protection	G	Dual-edged stress-response modulation	Important caution for antioxidant matrix use: NRF2 activation is favorable in normal-cell protection but may be undesirable in NRF2-addicted tumors.
13	Chemosensitization and radiosensitization	Chemo response ↑; radiation response ↑; apoptosis ↑; resistance pathways ↓	Chemo/radiation injury may ↓ in mucositis, dermatitis, and oxidative-stress contexts	R/G	Adjunct sensitization with possible normal-tissue protection	Attractive translational axis, but clinical evidence remains mainly pilot/small-study; interaction risk should be checked per regimen.
14	Clinical Translation Constraint	Free systemic exposure often insufficient for direct cytotoxic extrapolation from in-vitro micromolar data	Enhanced formulations may improve exposure but may also alter safety, liver-risk profile, and interaction potential	G	Bioavailability and formulation dominate translational interpretation	Separate ordinary curcumin, turmeric extract, piperine-enhanced, phytosomal, micellar, liposomal, nanoparticle, and IV/liposomal products where possible.

TSF legend:

P: 0–30 min

R: 30 min–3 hr

G: >3 hr

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
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



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



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



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



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



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



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

4415-

AgNPs,

SDT,

CUR,

Examining the Impact of Sonodynamic Therapy With Ultrasound Wave in the Presence of Curcumin-Coated Silver Nanoparticles on the Apoptosis of MCF7 Breast Cancer Cells

in-vitro,

BC,

MCF-7

29.3 ± 5.6 nm

 48.23 µg/ml

SDT was performed using an US frequency of 1 MHz, intensity of 2 W/cm2, and a distance of 2 cm.

tumCV↓, BAX↑, Casp3↑, Bcl-2↓, eff↑, ROS↑, sonoS↑, eff↑, MMP↓, Cyt‑c↑,

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,

Curc (200 mg/kg p. o.) and/or Lip acid (100 mg/kg i. p.)

rats

*hepatoP↑, *α-SMA↓, *COL3A1↓, *ROS↓, *GSH↑, *ALAT↓, *AST↓, *ALP↓, *MDA↓,

3514-

Bor,

CUR,

Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta

in-vivo,

AD,

rat

*DNAdam↓, *MDA↓, *AChE↓, *neuroP↑, *ROS↓, *NO↓,

6027-

CGA,

CUR,

EGCG,

QC,

RES

Contribution of Non-Coding RNAs to Anticancer Effects of Dietary Polyphenols: Chlorogenic Acid, Curcumin, Epigallocatechin-3-Gallate, Genistein, Quercetin and Resveratrol

Review,

Nor,

*ROS↓, ROS↑,

5995-

Chit,

CUR,

Enhancement of anticancer activity and drug delivery of chitosan-curcumin nanoparticle via molecular docking and simulation analysis

vitro+vivo,

Var,

eff↑, EPR↑, DNAdam↑, TumCCA↑, ROS↑, toxicity↓,

3628-

Cro,

VitE,

CUR,

Vitamin E, Turmeric and Saffron in Treatment of Alzheimer’s Disease

Review,

AD,

*antiOx↑, *ROS↓, *lipid-P↓, *Aβ↓, *AChE↓, *cognitive↑, *Inflam↓,

4826-

CUR,

The Bright Side of Curcumin: A Narrative Review of Its Therapeutic Potential in Cancer Management

Review,

Var,

*antiOx↑, *Inflam↑, *ROS↓, Apoptosis↑, TumCP↓, BioAv↓, Half-Life↓, eff↑, TumCCA↑, BAX↑, Bak↑, PUMA↑, BIM↑, NOXA↑, TRAIL↑, Bcl-2↓, Bcl-xL↓, survivin↓, XIAP↓, cMyc↓, Casp↑, NF-kB↓, STAT3↓, AP-1↓, angioG↓, TumMeta↑, VEGF↓, MMPs↓, DNMTs↓, HDAC↓, ROS↑,

4831-

CUR,

The dual role of curcumin and ferulic acid in counteracting chemoresistance and cisplatin-induced ototoxicity

in-vitro,

NA,

*NRF2↑, *P53↓, *NF-kB↓, ROS↑, Inflam↓, ChemoSen↑,

4828-

CUR,

Role of pro-oxidants and antioxidants in the anti-inflammatory and apoptotic effects of curcumin (diferuloylmethane)

Review,

Var,

*NF-kB↓, ROS↑,

4829-

CUR,

Dual Action of Curcumin as an Anti- and Pro-Oxidant from a Biophysical Perspective

Review,

Var,

*antiOx↑, ROS↑, *lipid-P↓, *iNOS↓, *BioAv↓,

4830-

CUR,

Curcumin and Its Derivatives Induce Apoptosis in Human Cancer Cells by Mobilizing and Redox Cycling Genomic Copper Ions

in-vitro,

Var,

eff↑, ROS↑, DNAdam↑, TumCG↓, Apoptosis↑, eff↓, Fenton↑, eff↑,

6218-

CUR,

Exploring the Thioredoxin System as a Therapeutic Target in Cancer: Mechanisms and Implications

Review,

Var,

NF-kB↓, TrxR↓, ROS↑, TumMeta↓, TumCD↑, RadioS↑, BioAv↝, BioAv↑,

6232-

CUR,

Rad,

Chemo,

The Effectiveness of Curcumin in Treating Oral Mucositis Related to Radiation and Chemotherapy: A Systematic Review

Review,

Var,

*VEGF↑, *Wound Healing↓, *NRF2↑, *Catalase↑, *SOD↑, *GSH↑, *ROS↓,

6230-

CUR,

Dual redox effects of 2,6-bis-(4-hydroxyl-3-methoxybenzylidene) cyclohexanone (BHMC) on human liver cancer cells, HepG2 via ROS, glutathione and Nrf2/Keap1 pathway

in-vitro,

Liver,

HepG2

chemoP↑, selectivity↑, *BioAv↓, *BioAv↑, ROS↑, ROS↓, ROS↑,

6227-

CUR,

Revisiting Curcumin in Cancer Therapy: Recent Insights into Molecular Mechanisms, Nanoformulations, and Synergistic Combinations

Review,

Var,

Wnt↓, β-catenin/ZEB1↓, PI3K↓, Akt↓, mTOR↓, JAK↓, STAT3↓, MAPK↓, NF-kB↓, NOTCH↓, TumCG↓, Apoptosis↑, GSK‐3β↓, cMyc↓, survivin↓, Axin2↑, TumCCA↑, PTEN↑, P53↑, ROS↑, Casp3↑, PARP↑, Ferroptosis↑, angioG↓, TumCI↓, TumMeta↓, BioAv↓, Half-Life↓, ChemoSen↑,

6225-

CUR,

Natural products for enhancing the sensitivity or decreasing the adverse effects of anticancer drugs through regulating the redox balance

Review,

Var,

ox-Trx1↑, TrxR1↓, TrxR↓, ROS↑, GSH/GSSG↓, eff↓, Fenton↑, H2O2↑, *NRF2↑, *Keap1↓, *HO-1↑, *NQO1↑, ChemoSen↑,

6223-

CUR,

Curcumin Rewires the Tumor Metabolic Landscape: Mechanisms and Clinical Prospects

Review,

Var,

Ferroptosis↑, GutMicro↑, Akt↓, mTOR↓, NF-kB↓, Wnt↓, β-catenin/ZEB1↓, STAT3↓, TumCP↓, TumCI↓, TumMeta↓, AMPK↑, P53↑, NRF2↑, TumCCA↑, Apoptosis↑, Casp↑, GPx4↓, DNMTs↓, HDAC↓, VEGF↓, Imm↑, NK cell↑, Warburg↓, Hif1a↓, HK2↓, PKM2↓, LDHA↓, GLUT1↓, MCT1↓, AMPK↑, FASN↓, SCD1↓, GLS↓, Apoptosis↑, ETC↓, MMP↓, ROS↑, lipid-P↑, ChemoSen↑, PDK1↓, Beclin-1↓, ATP↓, Glycolysis↓, GlucoseCon↓, lactateProd↑, MMPs↓, GSH↓, G6PD↓, OXPHOS↓, SREBP2↓, COX2↓, AP-1↓, NADH↓, NRF2↑, HO-1↑, Iron↑, MDA↑, *ROS↓, *Inflam↓,

6222-

CUR,

Anticancer Molecular Mechanisms of Curcuminoids: An Updated Review of Clinical Trials

Review,

Var,

RadioS↑, ChemoSen↑, MMPs↓, TumMeta↓, TumCI↓, Inflam↓, NF-kB↓, BioAv↓, BioAv↑, MAPK↓, PI3K↓, Akt↓, *ROS↓, *MDA↓, *lipid-P↓, *Half-Life↓, mTOR↓,

6221-

CUR,

Oxidative Stress and Cancer: Harnessing the Therapeutic Potential of Curcumin and Analogues Against Cancer

Review,

Var,

NF-kB↓, Imm↑, *TAC↑, *MDA↓, ROS↑, TumAuto↑, TumCCA↑, Keap1↑, ChemoSen↑, ER Stress↑, eff↓, TrxR↓, STAT3↓, *BioAv↓,

6217-

CUR,

Curcumin: a therapeutic strategy in cancers by inhibiting the canonical WNT/β-catenin pathway

Review,

Var,

Wnt↓, β-catenin/ZEB1↓, PPARγ↑, Akt↓, *ROS↓, *Inflam↓, Bcl-2↓, GSK‐3β↑, NF-kB↓, COX2↓,

6216-

CUR,

Role of Turmeric and Curcumin in Prevention and Treatment of Chronic Diseases: Lessons Learned from Clinical Trials

Review,

Var,

TumCG↓, angioG↓, EMT↓, TumCI↓, TumMeta↓, *GutMicro↑, *BioAv↓, *HO-1↑, *ROS↓, *COX2↓, *iNOS↓, PKCδ↓, EGFR↓, NF-kB↓, cJun↓, cFos↓, cMyc↓, Akt↓, PI3K↓, CDK4↓, *TNF-α↓, *CRP↓, *IL6↓, MMP9↓, VEGF↓, JAK↓, STAT↓, IL1↓, IL2↓, IL6↓, IL8↓, IL12↓, MCP1↓, Apoptosis↑, ER Stress↑, 5LO↓, XO↓, *NRF2↑, *HO-1↑, *AChE↓, *neuroP↑, *glucose↓, *GLUT2↑, *GLUT3↑, *GLUT4↑, *GlucoseCon↑, *AMPK↑, *BMD↑, *MDA↓, *eff↑, eff↑, P53↑, BAX↑, DNAdam↑, Bcl-2↓, CSCs↓, ALDH↓, CD133↑,

6215-

CUR,

Curcumin: biochemistry, pharmacology, advanced drug delivery systems, and its epigenetic role in combating cancer

Review,

Var,

*antiOx↑, *Inflam↓, *BioAv↓, NF-kB↓, PI3K↓, Akt↓, Wnt↓, β-catenin/ZEB1↓, DNMTs↓, TumCI↓, TumMeta↓, *BioAv↑, *BioAv↑, angioG↓, VEGF↓, MMPs↓, *ROS↓, *SOD↑, *Catalase↑, *GSTs↑, *HO-1↑, *NRF2↑, mTOR↓, GSK‐3β↓, FOXO1↓, *radioP↑, *IL1↓, *IL6↓, *TNF-α↓, HATs↓, HDAC↓, ROS↑, ROS↑, MMP↓, Casp↑, Cyt‑c↑, COX1↓, COX2↓, PGE2↓, *cytoP450↓, ChemoSen↑, cardioP↑, eff↑,

6214-

CUR,

Curcumin Nanoparticles-related Non-invasive Tumor Therapy, and Cardiotoxicity Relieve

TumCD↓, TumCI↓, *Inflam↓, *antiOx↓, *AntiTum↓, NF-kB↓, COX2↓, Casp9↓, ROS↑, BioAv↑, RadioS↑, ChemoSen↑, Imm↑, PhotoS↑, sonoS↑, 5LO↓, iNOS↓, IL2↓, TNF-α↓, Casp9↑, Casp3↑, Bcl-2↓, BAX↑, Apoptosis↑, ER Stress↑, cycD1/CCND1↓, CDK2↓, CycB/CCNB1↓, TumCCA↑, MMPs↓, *radioP↑, chemoP↑, hepatoP↑, cardioP↑, eff↑, PhotoS↑, eff↑, ROS↑, GSH↓,

6212-

CUR,

Rad,

Radiosensitization and Radioprotection by Curcumin in Glioblastoma and Other Cancers

Review,

Var,

RadioS↑, *radioP↑, EGFR↓, TGF-β↓, ROS↑, P53↑, PI3K↓, NF-kB↓, COX2↓, EMT↓, Hif1a↓, HSP90↓, mTOR↓, *Catalase↑, *SOD↑, *MDA↑, *Wound Healing↑, *hepatoP↑, *NF-kB↓, *ROS↓,

6210-

CUR,

Potential Roles and Mechanisms of Curcumin and its Derivatives in the Regulation of Ferroptosis

Ferroptosis↑, *Ferroptosis↓, ROS↑, Fenton↑, *IronCh↑, GPx4↓, MDA↑, GSH↓, *NRF2↑, *HO-1↑,

6207-

CUR,

Enhancing the Bioavailability and Bioactivity of Curcumin for Disease Prevention and Treatment

Review,

Var,

Review,

AD,

*AntiCan↑, *Obesity↓, *Inflam↓, *lipid-P↓, *BioAv↓, *BioAv↑, *BioAv↑, *BioAv↑, *BioAv↑, *BioAv↑, *ROS↓, *mt-SOD↑, *MDA↓, *BBB↓, *Aβ↓, *GSK‐3β↓, *tau↓, *neuroG↑, *memory↑, cardioP↑,

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,

*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↑,

2819-

CUR,

Chemo,

Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury

Review,

Var,

*hepatoP↑, *Inflam↓, *antiOx↑, *lipid-P↓, *GSH↑, *SOD↑, *Catalase↑, *GPx↑, *GSTs↑, *ROS↓, *ALAT↓, *AST↓, *MDA↓, *NRF2↑, *COX2↑, *NF-kB↓, *ICAM-1↓, *MCP1↓, *HO-1↑, CXCc↓,

2820-

CUR,

Hepatoprotective Effect of Curcumin on Hepatocellular Carcinoma Through Autophagic and Apoptic Pathways

in-vitro,

HCC,

HepG2

50 μM

*hepatoP↑, *ROS↓, tumCV↓,

2821-

CUR,

Antioxidant curcumin induces oxidative stress to kill tumor cells (Review)

Review,

Var,

*antiOx↑, *NRF2↑, *ROS↓, *Inflam↓, ROS↑, p‑ERK↑, ER Stress↑, mtDam↑, Apoptosis↑, Akt↓, mTOR↓, HO-1↑, Fenton↑, GSH↓, Iron↑, p‑JNK↑, Cyt‑c↑, ATF6↑, CHOP↑,

2816-

CUR,

NEUROPROTECTIVE EFFECTS OF CURCUMIN

Review,

AD,

Review,

Park,

*neuroP↑, *Inflam↓, *antiOx↑, *BioAv↓, *AP-1↓, *NF-kB↓, *HATs↓, *HDAC↑, Dose↑, *ROS↓, *cognitive↑, *Aβ↓,

2978-

CUR,

N-acetyl cysteine mitigates curcumin-mediated telomerase inhibition through rescuing of Sp1 reduction in A549 cells

in-vitro,

Lung,

A549

ROS↑, hTERT/TERT↓, Sp1/3/4↓, eff↓,

2980-

CUR,

Inhibition of NF B and Pancreatic Cancer Cell and Tumor Growth by Curcumin Is Dependent on Specificity Protein Down-regulation

in-vivo,

PC,

mice

TumCG↓, p50↓, p65↓, NF-kB↓, Sp1/3/4↓, MMP↓, ROS↑,

3574-

CUR,

The effect of curcumin (turmeric) on Alzheimer's disease: An overview

Review,

AD,

*antiOx↑, *Inflam↓, *lipid-P↓, *cognitive↑, *memory↑, *Aβ↓, *COX2↓, *ROS↓, *AP-1↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *SOD↑, *GSH↑, *HO-1↑, *IronCh↑, *BioAv↓, *Half-Life↝, *Dose↝, *BBB↑, *BioAv↑, *toxicity∅, *eff↑,

3576-

CUR,

Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease

Review,

AD,

*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↑,

2688-

CUR,

Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs

Review,

Var,

Review,

AD,

*ROS↓, *SOD↑, p16↑, JAK2↓, STAT3↓, CXCL12↓, IL6↓, MMP2↓, MMP9↓, TGF-β↓, α-SMA↓, LAMs↓, DNAdam↑, *memory↑, *cognitive↑, *Inflam↓, *antiOx↑, *NO↑, *MDA↓, *ROS↓, DNMT1↓, ROS↑, Casp3↑, Apoptosis↑, miR-21↓, LC3II↓, ChemoSen↑, NF-kB↓, CSCs↓, Nanog↓, OCT4↓, SOX2↓, eff↑, Sp1/3/4↓, miR-27a-3p↓, ZBTB10↑, SOX9?, ChemoSen↑, VEGF↓, XIAP↓, Bcl-2↓, cycD1/CCND1↓, BioAv↑, Hif1a↓, EMT↓, BioAv↓, PTEN↑, VEGF↓, Akt↑, EZH2↓, NOTCH1↓, TP53↑, NQO1↑, HO-1↑,

2308-

CUR,

Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells

in-vitro,

Liver,

HepG2

GlucoseCon↓, lactateProd↓, ECAR↓, NO↓, ROS↑, HK2↓, PFK1↓, GAPDH↓, PKM2↓, LDHA↓, FASN↓, GLUT1↓, MCT1↓, MCT4↓, HCAR1↓, SDH↑, ChemoSen↑, ROS↑, BioAv↑, P53↑, NF-kB↓, pH↑,

2312-

CUR,

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

Review,

Var,

ROS↑, PKM2↓,

2654-

CUR,

Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence

Review,

Var,

ROS↑, Catalase↓, SOD1↓, GLO-I↓, NADPH↓, TumCCA↑, Apoptosis↑, Akt↓, ER Stress↑, JNK↑, STAT3↓, BioAv↑,

3575-

CUR,

The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse

in-vivo,

AD,

mice

*antiOx↑, *ROS↓, *IL1β↓, *Aβ↓, *Inflam↓, *toxicity↓,

2810-

CUR,

Effect of curcuminoids on oxidative stress: A systematic review and meta-analysis of randomized controlled trials

Review,

Nor,

*SOD↑, *lipid-P↓, *GSH↑, *Catalase↑, *ROS↓,

3795-

CUR,

Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence

Review,

AD,

*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,

*GSK‐3β↓, *CDK5↓, *p‑tau↓, *IronCh↑, *ROS↓, *HO-1↑, *SOD↑, *Catalase↑, *GSH↑, *TNF-α↓, *IL6↓, *IL12↓, *NRF2↑, *PPARγ↑, *IL4↑, *AChE↓, *Dose↝, *GutMicro↑,

3753-

CUR,

Gala,

A Novel Galantamine–Curcumin Hybrid Inhibits Butyrylcholinesterase: A Molecular Dynamics Study

Study,

AD,

*BChE↓, *AChE↓, *Ach↑, *cognitive↑, *memory↑, *ROS↓, *Inflam↓, *NF-kB↓, *COX2?,

3831-

CUR,

Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s Disease

Review,

AD,

*neuroP↑, *ROS↓, *Ca+2↓, *MMP↑,

3748-

CUR,

RES,

Hup,

Riv,

Gala

Natural acetylcholinesterase inhibitors: A multi-targeted therapeutic potential in Alzheimer's disease

Review,

AD,

*AChE↓, *Inflam↓, *Aβ↓, *cognitive↑, *ROS↓,

3588-

CUR,

The effect of curcumin on cognition in Alzheimer’s disease and healthy aging: A systematic review of pre-clinical and clinical studies

Review,

AD,

*cognitive↝, *BioAv↑, *Inflam↓, *COX2↓, *iNOS↓, *NF-kB↓, *TNF-α↓, *IL1↓, *IL2↓, *IL6↓, *IL8↓, *IL12↓, *ROS↓, *RNS↓, *antiOx↑, *BBB↑, *BioAv↓, *cognitive↑, *memory↑, *tau↓, *eff↑,

3584-

CUR,

Curcumin in Health and Diseases: Alzheimer’s Disease and Curcumin Analogues, Derivatives, and Hybrids

*AChE↓, *Inflam↓, *antiOx↑, *Aβ↓, *ROS↓,

3579-

CUR,

AgNPs,

Metal–Curcumin Complexes in Therapeutics: An Approach to Enhance Pharmacological Effects of Curcumin

Review,

NA,

*IronCh↑, *BioAv↑, *antiOx↑, *Inflam↓, *BioAv↑, ROS↑, *neuroP↑, *eff↑,

3580-

CUR,

Curcumin Acts as Post-protective Effects on Rat Hippocampal Synaptosomes in a Neuronal Model of Aluminum-Induced Toxicity

in-vivo,

AD,

rat

*ROS↓, *Cyt‑c↓, *Casp3↓, *neuroP↑,

Showing Research Papers: 1 to 50 of 96
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 96

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 15, Catalase↑, 7, Ferroptosis↓, 1, GPx↑, 2, GSH↑, 8, GSR↓, 1, GSTs↑, 2, H2O2↓, 1, HO-1↑, 10, HO-2↓, 1, Keap1↓, 1, lipid-P↓, 9, MDA↓, 9, MDA↑, 1, MPO↓, 1, NQO1↑, 2, NRF2↑, 12, RNS↓, 1, ROS↓, 32, SOD↑, 10, mt-SOD↑, 1, TAC↑, 1,

Metal & Cofactor Biology ⓘ

Ferritin↑, 1, IronCh↑, 5,

Mitochondria & Bioenergetics ⓘ

AIF↓, 1, ATP↑, 1, MMP↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2, AMPK↑, 2, cytoP450↓, 1, glucose↓, 1, GlucoseCon↑, 1, GLUT2↑, 1, LDH↓, 1, LDL↓, 2, NADPH↓, 1, PPARγ↑, 1, SIRT1↑, 1,

Cell Death ⓘ

Akt↑, 1, Apoptosis↓, 1, Bcl-2↑, 1, Casp3↓, 2, Casp9↓, 1, Cyt‑c↓, 1, Ferroptosis↓, 1, iNOS↓, 4,

Transcription & Epigenetics ⓘ

Ach↑, 2, HATs↓, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1, P53↓, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 4, HDAC↑, 1, mTOR↓, 1, neuroG↑, 1, PI3K↑, 1, STAT↓, 1,

Migration ⓘ

AP-1↓, 2, Ca+2↓, 1, CDK5↓, 2, COL3A1↓, 1, TXNIP↓, 1, α-SMA↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 2, NO↑, 1, VEGF↑, 1,

Barriers & Transport ⓘ

BBB↓, 1, BBB↑, 3, GLUT3↑, 1, GLUT4↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2?, 1, COX2↓, 5, COX2↑, 1, CRP↓, 1, ICAM-1↓, 1, IL1↓, 2, IL10↑, 1, IL12↓, 2, IL17↓, 1, IL1β↓, 5, IL2↓, 2, IL23↓, 1, IL4↓, 1, IL4↑, 1, IL6↓, 5, IL8↓, 1, INF-γ↓, 1, Inflam↓, 20, Inflam↑, 1, MCP1↓, 2, NF-kB↓, 9, PGE2↓, 1, TNF-α↓, 7,

Synaptic & Neurotransmission ⓘ

AChE↓, 9, BChE↓, 1, BDNF↑, 1, ChAT↑, 1, tau↓, 3, p‑tau↓, 2,

Protein Aggregation ⓘ

Aβ↓, 9, BACE↓, 1, NLRP3↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 9, BioAv↑, 12, BioAv↝, 1, Dose↝, 2, eff↑, 4, Half-Life↓, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 2, ALP↓, 1, AST↓, 2, BMD↑, 1, CRP↓, 1, Ferritin↑, 1, GutMicro↑, 2, IL6↓, 5, LDH↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiCan↑, 1, AntiTum↓, 1, cardioP↑, 1, cognitive↑, 9, cognitive↝, 1, hepatoP↑, 4, memory↑, 7, neuroP↑, 9, Obesity↓, 1, OS↑, 1, radioP↑, 3, toxicity↓, 1, toxicity∅, 1, Wound Healing↓, 1, Wound Healing↑, 1,
Total Targets: 134

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

96 Curcumin
9 Resveratrol
6 Radiotherapy/Radiation
5 Quercetin
5 Chemotherapy
2 Silver-NanoParticles
2 EGCG (Epigallocatechin Gallate)
2 Galantamine
2 Ursolic acid
1 SonoDynamic Therapy UltraSound
1 Alpha-Lipoic-Acid
1 Boron
1 Chlorogenic acid
1 chitosan
1 Crocetin
1 Vitamin E
1 Huperzine A/Huperzia serrata
1 Rivastigmine
1 Ellagic acid
1 Cisplatin
1 Berberine
1 Melatonin
1 Silymarin (Milk Thistle) silibinin
1 5-fluorouracil
1 methylseleninic acid
1 Myricetin
1 Vitamin C (Ascorbic Acid)
1 Thymoquinone
1 salinomycin
1 Selenium
1 Selenium NanoParticles

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#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

Curcumin / ROS Cancer Research Results

Curcumin Cancer Mechanism Ranking

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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