Berberine / ROS Cancer Research Results

BBR, Berberine: Click to Expand ⟱
Features:

Berberine — Berberine is a protoberberine/isoquinoline alkaloid natural product found in plants such as Coptis, Berberis, and Phellodendron. It is a small-molecule phytochemical with pleiotropic metabolic, anti-inflammatory, and anticancer signaling effects rather than a single highly selective target profile. Its standard abbreviation is BBR. In oncology it is best classified as a multitarget natural-product lead compound and adjunct-sensitizer candidate, with strong preclinical evidence but no established standard anticancer regulatory use. Its translational profile is shaped by very low conventional oral bioavailability, extensive first-pass metabolism, broad tissue distribution, and substantial context dependence between cancer-cell pro-death effects and normal-cell cytoprotective redox effects.

Primary mechanisms (ranked):

  1. AMPK-centered metabolic stress with mitochondrial dysfunction, ATP depletion, and apoptosis/autophagy induction
  2. Suppression of aerobic glycolysis and hypoxia signaling, including HIF-1α, GLUT1, HK2, LDHA, and PKM2-linked tumor metabolism
  3. Anti-proliferative cell-cycle control with cyclin/CDK suppression and tumor suppressor reactivation
  4. Inhibition of PI3K/AKT, MAPK/ERK, JAK/STAT, and NF-κB inflammatory-survival signaling
  5. Anti-metastatic and anti-EMT activity via Wnt/β-catenin, TGF-β/Smad, FAK/RhoA/ROCK, MMPs, and CXCR4-related programs
  6. Pro-oxidant mitochondrial ROS elevation and ER-stress/caspase signaling in many cancer models, with opposite antioxidant/NRF2-supportive effects in some normal-cell and non-cancer settings
  7. Context-dependent chemosensitization and radiosensitization, including effects on hypoxia signaling and DNA-repair competence
  8. Emerging ferroptosis-related activity in some tumor models, but not a universal dominant mechanism across berberine biology

Bioavailability / PK relevance: Conventional oral berberine has poor systemic bioavailability, often cited as below 1% in animal studies, because of limited absorption, P-glycoprotein efflux, first-pass intestinal/hepatic metabolism, and self-aggregation. Human exposure is usually in the low ng/mL plasma range with conventional dosing, while multiple metabolites may contribute to activity. Tissue distribution can exceed plasma levels, but PK remains a major clinical translation constraint.

In-vitro vs systemic exposure relevance: Many anticancer in-vitro studies use roughly 10–100 µM, commonly around 20–50 µM, which usually exceeds readily achievable conventional plasma exposure after standard oral dosing. Therefore, direct translation of cell-culture potency to systemic monotherapy expectations is limited unless local gut exposure, tissue accumulation, metabolite contribution, formulation enhancement, or combination use is specifically relevant.

Clinical evidence status: Strong preclinical and mechanistic evidence; limited early human oncology/chemoprevention evidence; no established phase III anticancer efficacy standard and no mainstream regulatory approval as an anticancer drug. Current clinical relevance is best viewed as investigational and adjunct-oriented rather than proven standalone oncology therapy.

Berberine is a chemical found in some plants like European barberry, goldenseal, goldthread, Oregon grape, phellodendron, and tree turmeric. Berberine is a bitter-tasting and yellow-colored chemical.
Coptis (commonly referring to Coptidis Rhizoma, a traditional Chinese medicinal herb) contains bioactive alkaloids (most notably berberine and coptisine) that have been studied for their pharmacological effects—including their influence on reactive oxygen species (ROS) and related pathways.

– Berberine is known for its relatively low oral bioavailability, often cited at less than 1%. This low bioavailability is mainly due to poor intestinal absorption and active efflux by transport proteins such as P-glycoprotein.
– Despite the low bioavailability, berberine is still pharmacologically active, and its metabolites may also contribute to its overall effects.

• Effective Dosage in Studies
– Many clinical trials or preclinical studies use dosages in the range of 500 to 1500 mg per day, typically administered in divided doses.
– Therefore, to obtain a bioactive dose of berberine, supplementation in a standardized extract form is necessary.

-IC50 in cancer cell lines: Approximately 10–100 µM (commonly around 20–50 µM in many models)
-IC50 in normal cell lines: Generally higher (often above 100 µM), although this can vary with cell type
- In vivo studies: Dosing regimens in animal models generally range from about 50 to 200 mg/kg
- very effective AChE inhibitor (Alzheimers)
- Berberine may enhance the effects of blood-thinning medications like warfarin and aspirin.


-Note half-life reports vary 2.5-90hrs?.
-low solubility of apigenin in water : BioAv
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- PI3K/AKT(Inhibition), JAK/STATs, Wnt/β-catenin, AMPK, MAPK/ERK, and JNK.
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, EZH2↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi1↓, CD133↓, β-catenin↓, n-myc↓, sox2↓, notch2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, α↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 AMPK → mTOR axis ↑ AMPK / ↓ mTOR signaling Metabolic stress + growth suppression In vivo/in vitro colon tumorigenesis model: berberine activates AMPK, inhibits mTOR signaling and reduces proliferation/tumorigenesis, growth suppression, autophagy, HIF-1α ↓, glycolysis ↓, berberine’s known mitochondrial/energetic effects (ref)
2 Mitochondrial dysfunction / ROS generation ↑ ROS / mitochondrial stress Upstream metabolic trigger Berberine inhibits mitochondrial function, increases ROS, and contributes to AMPK activation and downstream apoptosis (ref)
3 Mitochondrial apoptosis (cytochrome c release) ↑ cytochrome c release Intrinsic death signaling Oral cancer model: berberine reduces mitochondrial membrane potential, releases cytochrome c, activates caspase-3 (ref)
4 Intrinsic apoptosis (caspase-3 activation) ↑ caspase-3 activation Programmed cell death Same oral cancer study documents caspase-3 activation as a key execution marker (ref)
5 NF-κB signaling (p65 activation) ↓ NF-κB activation Reduced pro-survival transcription Colon cancer model reports inhibition of p65 phosphorylation; interpreted as secondary to metabolic/redox stress (ref)
6 Cell cycle control ↑ G1 arrest Proliferation blockade Prostate cancer model: berberine induces G1-phase cell cycle arrest and caspase-3–dependent apoptosis (ref)
7 Hypoxia / glycolysis signaling (HIF-1α) ↓ HIF-1α protein Warburg / glycolysis suppression Berberine suppresses mTOR and reduces HIF-1α protein expression downstream of AMPK activation (ref)
8 Angiogenesis signaling (HIF-1α → VEGF axis) ↓ VEGF signaling Reduced vascular support Lung cancer study: berberine suppresses VEGF signaling alongside HIF-1α inhibition (ref)
9 PI3K–AKT–mTOR signaling ↓ PI3K / AKT / mTOR Survival pathway suppression Gastric cancer paper: berberine represses PI3K/AKT/mTOR signaling and improves chemosensitivity (ref)
10 Migration / invasion programs ↓ migration & invasion Anti-metastatic phenotype Tongue SCC model: berberine suppresses migration and invasion with associated signaling changes (ref)
11 Telomerase (hTERT) / immortalization axis ↓ hTERT-related signaling Reduced proliferative capacity Lung cancer study includes AP-2/hTERT regulatory axis modulation by berberine (ref)
12 In vivo tumor suppression ↓ tumorigenesis Demonstrated anti-tumor effect Colon tumorigenesis model confirms reduced proliferation and tumor burden with berberine (ref)


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


Scientific Papers found: Click to Expand⟱
2699- BBR,    Plant Isoquinoline Alkaloid Berberine Exhibits Chromatin Remodeling by Modulation of Histone Deacetylase To Induce Growth Arrest and Apoptosis in the A549 Cell Line
- in-vitro, Lung, A549
HDAC↓, TumCCA↑, TNF-α↓, COX2↓, MMP2↓, MMP9↓, P21↑, P53↑, Casp↑, ac‑H3↑, ac‑H4↑, ROS↑, MMP↓,
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↓,
2686- BBR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Nor, NA
Inflam↓, IL6↓, MCP1↓, COX2↓, PGE2↓, MMP2↓, MMP9↓, DNAdam↑, eff↝, Telomerase↓, Bcl-2↓, AMPK↑, ROS↑, MMP↓, ATP↓, p‑mTORC1↓, p‑S6K↓, ERK↓, PI3K↓, PTEN↑, Akt↓, Raf↓, MEK↓, Dose↓, Dose↑, selectivity↑, TumCCA↑, eff↑, EGFR↓, Glycolysis↓, Dose?, p27↑, CDK2↓, CDK4↓, cycD1/CCND1↓, cycE/CCNE↓, Bax:Bcl2↑, Casp3↑, Casp9↑, VEGFR2↓, ChemoSen↑, eff↑, eff↑, PGE2↓, JAK2↓, STAT3↓, CXCR4↓, CCR7↓, uPA↓, CSCs↓, EMT↓, Diff↓, CD133↓, Nestin↓, n-MYC↓, NOTCH↓, SOX2↓, Hif1a↓, VEGF↓, RadioS↑,
5177- BBR,    Berberine induces apoptosis in human HSC-3 oral cancer cells via simultaneous activation of the death receptor-mediated and mitochondrial pathway
- in-vitro, Oral, HMC3
TumCCA↑, Apoptosis↑, TumCG↓, Casp3↑, TumCCA↑, ROS↑, Ca+2↑, MMP↓, ER Stress↑, Cyt‑c↑,
4299- BBR,    Berberine attenuates cognitive impairment and ameliorates tau hyperphosphorylation by limiting the self-perpetuating pathogenic cycle between NF-κB signaling, oxidative stress and neuroinflammation
- in-vivo, AD, NA
*memory↑, *p‑tau↓, *NF-kB↓, *GSH↑, *lipid-P↓, *cognitive↑, *ROS↓, *Inflam↓,
3684- BBR,    Neuroprotective effects of berberine in animal models of Alzheimer’s disease: a systematic review of pre-clinical studies
- Review, AD, NA
*Inflam↓, *antiOx↓, *AChE↓, *BChE↓, *MAOA↓, *MAOB↓, *lipid-P↓, *GSH↑, *ROS↓, *APP↓, *BACE↓, *p‑tau↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *MAPK↓, *PI3K↓, *Akt↓, *neuroP↑, *memory↑,
3680- BBR,    Network pharmacology reveals that Berberine may function against Alzheimer’s disease via the AKT signaling pathway
- in-vivo, AD, NA
*Akt↑, *neuroP↑, *p‑ERK↑, *Aβ↓, *Inflam↓, *ROS↓, *BioAv↑, *BBB↑, *Half-Life↝, *memory↑, *cognitive↑, *HSP90↑, *APP↓, *mTOR↓, *P70S6K↓, *CD31↑, *VEGF↑, *N-cadherin↑, *Apoptosis↓,
3679- BBR,    Berberine alleviates Alzheimer's disease by activating autophagy and inhibiting ferroptosis through the JNK-p38MAPK signaling pathway
- in-vivo, AD, NA
*Beclin-1↑, *LC3B↑, *p62↓, *ROS↓, *lipid-P↓, *MDA↓, *Ferroptosis↓, *TfR1/CD71↓, *FTH1↑, *memory↑, *JNK↓, *p38↓, *Aβ↓, *Inflam↓,
3678- BBR,    Network pharmacology study on the mechanism of berberine in Alzheimer’s disease model
- Review, AD, NA
*APP↓, *PPARγ↑, *NF-kB↓, *Aβ↓, *cognitive↑, *antiOx↑, *Inflam↓, *Apoptosis↓, *BioAv↑, *BioAv↝, *BBB↑, *motorD↑, *NRF2↑, *HO-1↑, *ROS↓, *p‑Akt↑, *p‑ERK↑,
3677- BBR,    Berberine: A Potential Multipotent Natural Product to Combat Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, *AChE↓, *BChE↓, *MAOA↓, *Aβ↓, *LDL↓, *ROS↓, *RNS↓, *lipid-P↓, *Dose↝, *MAOB↓, *memory↑, *toxicity↓, *BBB↑,
1379- BBR,    Berberine derivative DCZ0358 induce oxidative damage by ROS-mediated JNK signaling in DLBCL cells
- in-vitro, lymphoma, NA
TumCP↓, CDK4↓, CDK6↓, cycD1/CCND1↓, TumCCA↑, MMP↓, Ca+2↑, ATP↓, mtDam↑, Apoptosis↑, ROS↑, JNK↑, eff↓,
1396- BBR,    Berberine induced down-regulation of matrix metalloproteinase-1, -2 and -9 in human gastric cancer cells (SNU-5) in vitro
- in-vitro, GC, SNU1041 - in-vitro, GC, SNU5
tumCV↓, ROS↑, MMP1↓, MMP2↓, MMP9↓, MMP7∅,
1394- BBR,  DL,    Synergistic Inhibitory Effect of Berberine and d-Limonene on Human Gastric Carcinoma Cell Line MGC803
- in-vitro, GC, MGC803
eff↑, ROS↑, MMP↓, Casp3↑, Bcl-2↓, TumCCA↑,
1393- BBR,  EPI,    Berberine promotes antiproliferative effects of epirubicin in T24 bladder cancer cells by enhancing apoptosis and cell cycle arrest
- in-vitro, Bladder, T24/HTB-9
ChemoSen↑, TumCCA↑, Apoptosis↑, cl‑Casp3↑, cl‑Casp9↑, BAX↑, P53↑, P21↑, Bcl-2↓, ROS↑,
1392- BBR,    Based on network pharmacology and experimental validation, berberine can inhibit the progression of gastric cancer by modulating oxidative stress
- in-vitro, GC, AGS - in-vitro, GC, MKN45
TumCG↓, TumCMig↓, ROS↑, MDA↑, SOD↓, NRF2↓, HO-1↓, Hif1a↓, EMT↓, Snail↓, Vim↓,
1390- BBR,  Rad,    Berberine Inhibited Radioresistant Effects and Enhanced Anti-Tumor Effects in the Irradiated-Human Prostate Cancer Cells
- in-vitro, Pca, PC3
RadioS↑, Apoptosis↑, ROS↑, eff↑, BAX↑, Casp3↑, P53↑, p38↑, JNK↑, Bcl-2↓, ERK↓, HO-1↓,
1389- BBR,  Lap,    Berberine reverses lapatinib resistance of HER2-positive breast cancer cells by increasing the level of ROS
- in-vitro, BC, BT474 - in-vitro, BC, AU-565
ChemoSen↑, Apoptosis↑, ROS↑, NRF2↓,
1387- BBR,    Antitumor Activity of Berberine by Activating Autophagy and Apoptosis in CAL-62 and BHT-101 Anaplastic Thyroid Carcinoma Cell Lines
- in-vitro, Thyroid, CAL-62
TumCG↓, Apoptosis↑, LC3B↑, ROS↑, PI3K↓, Akt↓, mTOR↓,
1386- BBR,    Berberine-induced apoptosis in human breast cancer cells is mediated by reactive oxygen species generation and mitochondrial-related apoptotic pathway
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
tumCV↓, ROS↑, JNK↑, MMP↓, Bcl-2↓, BAX↑, Cyt‑c↑, AIF↝,
1385- BBR,  5-FU,    Low-Dose Berberine Attenuates the Anti-Breast Cancer Activity of Chemotherapeutic Agents via Induction of Autophagy and Antioxidation
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
eff↓, ROS↑, TumCP↑, NRF2↑, ChemoSen↓,
1384- BBR,    Berberine induces apoptosis via ROS generation in PANC-1 and MIA-PaCa2 pancreatic cell lines
- in-vitro, PC, PANC1
TumCCA↑, ROS↑, Apoptosis↑,
1382- BBR,    Berberine increases the expression of cytokines and proteins linked to apoptosis in human melanoma cells
- in-vitro, Melanoma, SK-MEL-28
Apoptosis↑, necrosis↑, DNAdam↑, TumCCA↑, ROS↑, Casp3↑, p‑P53↑, ERK↑,
1381- BBR,  Rad,    Berberine enhances the sensitivity of radiotherapy in ovarian cancer cell line (SKOV-3)
- in-vitro, Ovarian, SKOV3
RadioS↑, ROS↑, GSH↓, Apoptosis↑,
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↑,
1395- BBR,    Analysis of the mechanism of berberine against stomach carcinoma based on network pharmacology and experimental validation
- in-vitro, GC, NA
Apoptosis↑, ROS↑, MMP↓, ATP↓, AMPK↑, TP53↑, p‑MAPK↓, p‑ERK↓,
1377- BBR,    Berberine inhibits autophagy and promotes apoptosis of fibroblast-like synovial cells from rheumatoid arthritis patients through the ROS/mTOR signaling pathway
- in-vitro, Arthritis, NA
Apoptosis↑, MMP↓, Bax:Bcl2↑, LC3‑Ⅱ/LC3‑Ⅰ↓, p62↑, *ROS↓,
1376- BBR,  immuno,    Berberine sensitizes immune checkpoint blockade therapy in melanoma by NQO1 inhibition and ROS activation
- in-vivo, Melanoma, NA
OS↑, ROS↑, NQO1↓, ICD↑,
1375- BBR,    13-[CH2CO-Cys-(Bzl)-OBzl]-Berberine: Exploring The Correlation Of Anti-Tumor Efficacy With ROS And Apoptosis Protein
- in-vitro, CRC, HCT8 - in-vivo, NA, NA
ROS↑, TumCP↓, XIAP↓, TumCG↓, *toxicity↓,
1374- BBR,  PDT,    Berberine associated photodynamic therapy promotes autophagy and apoptosis via ROS generation in renal carcinoma cells
- in-vitro, RCC, 786-O - in-vitro, RCC, HK-2
ROS↑, TumAuto↑, Apoptosis↑, Casp3↑, eff↑,
1299- BBR,    Effects of Berberine and Its Derivatives on Cancer: A Systems Pharmacology Review
- Review, NA, NA
TumCCA↑, TP53↑, COX2↓, Bax:Bcl2↑, ROS↑, VEGFR2↓, Akt↓, ERK↓, MMP2↓, MMP9↓, IL8↑, P21↑, p27↑, E-cadherin↓, Fibronectin↓, cMyc↓,
2681- BBR,  PDT,    Berberine-photodynamic induced apoptosis by activating endoplasmic reticulum stress-autophagy pathway involving CHOP in human malignant melanoma cells
- in-vitro, Melanoma, NA
Apoptosis↑, cl‑Casp3↑, LC3s↑, ER Stress↑, ROS↑, CHOP↑,
2680- BBR,  PDT,    Photodynamic therapy-triggered nuclear translocation of berberine from mitochondria leads to liver cancer cell death
- in-vitro, Liver, HUH7
TumCD↑, ROS↑, TumCCA↑, ER Stress↑,
2679- BBR,    Berberine Improves Behavioral and Cognitive Deficits in a Mouse Model of Alzheimer’s Disease via Regulation of β-Amyloid Production and Endoplasmic Reticulum Stress
- in-vivo, AD, NA
*cognitive↑, PERK↓, *eIF2α↓, *neuroP↑, *ER Stress↓, *ROS↓,
2677- BBR,    Liposome-Encapsulated Berberine Alleviates Liver Injury in Type 2 Diabetes via Promoting AMPK/mTOR-Mediated Autophagy and Reducing ER Stress: Morphometric and Immunohistochemical Scoring
- in-vivo, Diabetic, NA
*hepatoP↑, *LC3II↑, *Beclin-1↑, *AMPK↑, *mTOR↑, *ER Stress↓, *CHOP↓, *JNK↓, *ROS↓, *Inflam↓, *BG↓, *SOD↑, *GPx↑, *Catalase↑, *IL10↑, *IL6↓, *TNF-α↓, *ALAT↓, *AST↓, *ALP↓,
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↓,
2674- BBR,    Berberine: A novel therapeutic strategy for cancer
- Review, Var, NA - Review, IBD, NA
Inflam↓, AntiCan↑, Apoptosis↑, TumAuto↑, TumCCA↑, TumMeta↓, TumCI↓, eff↑, eff↑, CD4+↓, TNF-α↓, IL1↓, BioAv↓, BioAv↓, other↓, AMPK↑, MAPK↓, NF-kB↓, IL6↓, MCP1↓, PGE2↓, COX2↓, *ROS↓, *antiOx↑, *GPx↑, *Catalase↑, AntiTum↑, TumCP↓, angioG↓, Fas↑, FasL↑, ROS↑, ATM↑, P53↑, RB1↑, Casp9↑, Casp8↑, Casp3↓, BAX↑, Bcl-2↓, Bcl-xL↓, IAP1↓, XIAP↓, survivin↓, MMP2↓, MMP9↓, CycB/CCNB1↓, CDC25↓, CDC25↓, Cyt‑c↑, MMP↓, RenoP↑, mTOR↓, MDM2↓, LC3II↑, ERK↓, COX2↓, MMP3↓, TGF-β↓, EMT↑, ROCK1↓, FAK↓, RAS↓, Rho↓, NF-kB↓, uPA↓, MMP1↓, MMP13↓, ChemoSen↑,
1397- BBR,  Chemo,    Effects of Coptis extract combined with chemotherapeutic agents on ROS production, multidrug resistance, and cell growth in A549 human lung cancer cells
- in-vitro, Lung, A549
TumCG↓, ROS↑, MDR1↓,
2023- BBR,    Berberine Induces Caspase-Independent Cell Death in Colon Tumor Cells through Activation of Apoptosis-Inducing Factor
- in-vitro, Colon, NA - in-vitro, Nor, YAMC
TumCD↑, *toxicity↓, selectivity↑, ROS↑, *ROS∅, MMP↓, *MMP∅, PARP↑, BioAv↝,
2021- BBR,    Berberine: An Important Emphasis on Its Anticancer Effects through Modulation of Various Cell Signaling Pathways
- Review, NA, NA
*antiOx?, *Inflam↓, Apoptosis↑, TumCCA↑, BAX↑, eff↑, VEGF↓, PI3K↓, Akt↓, mTOR↓, Telomerase↓, β-catenin/ZEB1↓, Wnt↓, EGFR↓, AP-1↓, NF-kB↓, COX2↑, NRF2↓, RadioS↑, STAT3↓, ERK↓, AR↓, ROS↑, eff↑, selectivity↑, selectivity↑, BioAv↓, DNMT1↓, cMyc↓,
1405- BBR,  Chit,    Chitosan/alginate nanogel potentiate berberine uptake and enhance oxidative stress mediated apoptotic cell death in HepG2 cells
- in-vitro, Liver, HepG2
*BioAv↑, ROS↑, MMP↓, TumCP↓,
1404- BBR,    Berberine-induced apoptosis in human prostate cancer cells is initiated by reactive oxygen species generation
- in-vitro, Pca, PC3
Apoptosis↑, *Apoptosis∅, MMP↓, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, ROS↑, eff↓, Cyt‑c↑,
1402- BBR,    Berberine-induced apoptosis in human glioblastoma T98G cells is mediated by endoplasmic reticulum stress accompanying reactive oxygen species and mitochondrial dysfunction
- in-vitro, GBM, T98G
tumCV↓, ROS↑, Ca+2↑, ER Stress↑, eff↓, Bax:Bcl2↑, MMP↓, Casp9↑, Casp3↑, cl‑PARP↑,
1401- BBR,    Berberine induces apoptosis in glioblastoma multiforme U87MG cells via oxidative stress and independent of AMPK activity
- in-vitro, GBM, U87MG
TumCP↓, Apoptosis↑, ROS↑,
1400- BBR,    Set9, NF-κB, and microRNA-21 mediate berberine-induced apoptosis of human multiple myeloma cells
- in-vitro, Melanoma, U266
ROS↑, TumCCA↑, Apoptosis↑, miR-21↓, Bcl-2↓, NF-kB↓, Set9↑,
1399- BBR,  Rad,    Radiotherapy Enhancing and Radioprotective Properties of Berberine: A Systematic Review
- Review, NA, NA
*ROS↓, *MDA↓, *TNF-α↓, *TGF-β↓, *IL10↑, ROS↑, DNAdam↑, mtDam↑, MMP↓, Apoptosis↑, TumCCA↑, Hif1a↓, VEGF↓, RadioS↑,
1398- BBR,    Berberine inhibits the progression of renal cell carcinoma cells by regulating reactive oxygen species generation and inducing DNA damage
- in-vitro, Kidney, NA
TumCP↓, TumCMig↓, ROS↑, Apoptosis↑, BAX↑, BAD↑, Bak↑, Cyt‑c↑, cl‑Casp3↑, cl‑Casp9↑, E-cadherin↑, TIMP1↑, γH2AX↑, Bcl-2↓, N-cadherin↓, Vim↓, Snail↓, RAD51↓, PCNA↓,
1383- CUR,  BBR,  RES,    Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases
- Review, NA, NA
GSK‐3β↝, ROS↑,
1391- RES,  BBR,    Effects of Resveratrol, Berberine and Their Combinations on Reactive Oxygen Species, Survival and Apoptosis in Human Squamous Carcinoma (SCC-25) Cells
- in-vitro, Tong, SCC25
ROS↑, eff↑,
1403- SDT,  BBR,    From 2D to 3D In Vitro World: Sonodynamically-Induced Prooxidant Proapoptotic Effects of C60-Berberine Nanocomplex on Cancer Cells
- in-vitro, Cerv, HeLa - in-vitro, Lung, LLC1
eff↑, tumCV↓, ATP↓, ROS↑, Casp3↑, Casp7↑, mtDam↑,

Showing Research Papers: 1 to 49 of 49

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 49

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   HO-1↓, 2,   ICD↑, 1,   MDA↑, 1,   NQO1↓, 1,   NRF2↓, 3,   NRF2↑, 1,   ROS↑, 37,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↝, 1,   ATP↓, 4,   CDC25↓, 2,   MEK↓, 1,   MMP↓, 14,   mtDam↑, 3,   Raf↓, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 3,   cMyc↓, 2,   Glycolysis↓, 1,   p‑S6K↓, 1,  

Cell Death ⓘ

Akt↓, 4,   Apoptosis↑, 20,   BAD↑, 1,   Bak↑, 1,   BAX↑, 6,   Bax:Bcl2↑, 4,   Bcl-2↓, 8,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↓, 1,   Casp3↑, 8,   cl‑Casp3↑, 4,   Casp7↑, 1,   Casp8↑, 1,   Casp9↑, 3,   cl‑Casp9↑, 3,   Cyt‑c↑, 5,   Fas↑, 1,   FasL↑, 1,   IAP1↓, 1,   JNK↑, 3,   MAPK↓, 1,   p‑MAPK↓, 1,   MDM2↓, 1,   necrosis↑, 1,   p27↑, 2,   p38↑, 1,   Set9↑, 1,   survivin↓, 1,   Telomerase↓, 2,   TumCD↑, 2,  

Transcription & Epigenetics ⓘ

ac‑H3↑, 1,   ac‑H4↑, 1,   miR-21↓, 1,   other↓, 1,   tumCV↓, 4,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   CHOP↑, 1,   ER Stress↑, 4,   PERK↓, 1,  

Autophagy & Lysosomes ⓘ

LC3‑Ⅱ/LC3‑Ⅰ↓, 1,   LC3B↑, 1,   LC3II↑, 1,   LC3s↑, 1,   p62↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

ATM↑, 1,   DNAdam↑, 3,   DNMT1↓, 1,   P53↑, 4,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 2,   PCNA↓, 1,   RAD51↓, 1,   TP53↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 2,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↑, 3,   RB1↑, 1,   TumCCA↑, 15,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CSCs↓, 1,   Diff↓, 1,   EMT↓, 2,   EMT↑, 1,   ERK↓, 5,   ERK↑, 1,   p‑ERK↓, 1,   GSK‐3β↝, 1,   HDAC↓, 1,   mTOR↓, 3,   p‑mTORC1↓, 1,   n-MYC↓, 1,   Nestin↓, 1,   NOTCH↓, 1,   PI3K↓, 3,   PTEN↑, 1,   RAS↓, 1,   SOX2↓, 1,   STAT3↓, 2,   TumCG↓, 5,   Wnt↓, 1,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 3,   E-cadherin↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   Fibronectin↓, 1,   MMP1↓, 2,   MMP13↓, 1,   MMP2↓, 5,   MMP3↓, 1,   MMP7∅, 1,   MMP9↓, 5,   N-cadherin↓, 1,   Rho↓, 1,   ROCK1↓, 1,   Snail↓, 2,   TGF-β↓, 1,   TIMP1↑, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 6,   TumCP↑, 1,   TumMeta↓, 1,   uPA↓, 2,   Vim↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 2,   Hif1a↓, 3,   VEGF↓, 3,   VEGFR2↓, 2,  

Immune & Inflammatory Signaling ⓘ

CCR7↓, 1,   CD4+↓, 1,   COX2↓, 5,   COX2↑, 1,   CXCR4↓, 1,   IL1↓, 1,   IL6↓, 2,   IL8↑, 1,   Inflam↓, 2,   JAK2↓, 1,   MCP1↓, 2,   NF-kB↓, 4,   PGE2↓, 3,   TNF-α↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 3,   BioAv↝, 1,   ChemoSen↓, 1,   ChemoSen↑, 4,   Dose?, 1,   Dose↓, 1,   Dose↑, 1,   eff↓, 4,   eff↑, 12,   eff↝, 1,   MDR1↓, 1,   RadioS↑, 5,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 2,   IL6↓, 2,   TP53↑, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   OS↑, 1,   RenoP↑, 1,  
Total Targets: 176

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx?, 1,   antiOx↓, 1,   antiOx↑, 3,   Catalase↑, 2,   Ferroptosis↓, 1,   GPx↑, 2,   GSH↑, 3,   HO-1↑, 2,   lipid-P↓, 5,   MDA↓, 3,   NRF2↑, 2,   RNS↓, 1,   ROS↓, 14,   ROS∅, 1,   SOD↑, 3,  

Metal & Cofactor Biology ⓘ

FTH1↑, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP∅, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   AMPK↑, 1,   LDL↓, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   p‑Akt↑, 1,   Apoptosis↓, 2,   Apoptosis∅, 1,   BAX↓, 1,   cl‑Casp3↓, 1,   Ferroptosis↓, 1,   JNK↓, 2,   MAPK↓, 1,   p38↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   eIF2α↓, 1,   p‑eIF2α↓, 1,   ER Stress↓, 3,   HSP90↑, 1,   p‑PERK↓, 1,   UPR↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 2,   LC3B↑, 1,   LC3II↑, 1,   p62↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 2,   mTOR↓, 1,   mTOR↑, 1,   P70S6K↓, 1,   PI3K↓, 1,   STAT3↑, 1,  

Migration ⓘ

APP↓, 3,   Ca+2↓, 1,   CD31↑, 1,   N-cadherin↑, 1,   TGF-β↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↓, 1,   VEGF↑, 1,  

Barriers & Transport ⓘ

BBB↑, 3,  

Immune & Inflammatory Signaling ⓘ

IL10↑, 2,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 7,   JAK2↑, 1,   NF-kB↓, 3,   TNF-α↓, 3,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   BChE↓, 2,   MAOA↓, 2,   p‑tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 4,   BACE↓, 1,   MAOB↓, 2,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   BG↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 4,   hepatoP↑, 1,   memory↑, 5,   motorD↑, 1,   neuroP↑, 4,   toxicity↓, 3,  
Total Targets: 90

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
49 Berberine
3 Radiotherapy/Radiation
3 Photodynamic Therapy
2 Resveratrol
1 D-limonene
1 epirubicin
1 Lapatinib
1 5-fluorouracil
1 doxorubicin
1 immunotherapy
1 Chemotherapy
1 chitosan
1 Curcumin
1 SonoDynamic Therapy UltraSound
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#:41  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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