Cynara scolymus/Globe Artichoke/Artichoke Extract / ROS Cancer Research Results

CS, Cynara scolymus/Globe Artichoke/Artichoke Extract: Click to Expand ⟱
Features:

Cynara scolymus - Globe Artichoke / Artichoke Extract,, Artichoke leaf extract

Type: Botanical extract / polyphenol-rich medicinal plant

Active Constituents: Cynarin, chlorogenic acid, caffeoylquinic acids, luteolin, apigenin, and related flavonoids and phenolic compounds.

Function: Cynara scolymus exhibits antioxidant, anti-inflammatory, hepatoprotective, lipid-modulating, metabolic, and cytoprotective effects. Artichoke extracts can modulate oxidative stress, inflammatory signaling, apoptosis, and cellular metabolism.

Cancer: Experimental studies indicate antiproliferative, pro-apoptotic, antioxidant, and anti-inflammatory effects in multiple cancer cell models, with potential modulation of cell-cycle and survival pathways.

Alzheimer's Disease: Preclinical evidence suggests neuroprotective effects through antioxidant, anti-inflammatory, and cholinergic mechanisms, but the evidence base is less developed than for its metabolic and hepatic effects.


For supplements look for: standardized caffeoylquinic acids per capsule (example 5%, 25mg/capsule)

Cynara scolymus — globe artichoke, commonly used medicinally as artichoke leaf extract (ALE), is a polyphenol- and sesquiterpene-lactone-rich botanical preparation derived primarily from the leaves of Cynara cardunculus L. subsp. scolymus, historically also designated Cynara scolymus L. It is classified as a botanical extract / herbal medicinal product rather than a single defined drug. Common abbreviations are CS and ALE. Major constituents include chlorogenic acid and other caffeoylquinic acids, cynarin, luteolin glycosides, apigenin derivatives, and the sesquiterpene lactone cynaropicrin; their concentrations vary substantially with plant part, cultivar, extraction method, and standardization. Artichoke leaf preparations have established traditional gastrointestinal use and human clinical investigation for dyslipidemia and metabolic/liver disorders, whereas anticancer activity remains predominantly preclinical.

Primary mechanisms (ranked):

  1. Induction of mitochondrial apoptosis through ↑BAX, ↓BCL-2, mitochondrial dysfunction, and caspase-9/caspase activation.
  2. Cell-cycle arrest and durable growth suppression, including G2/M arrest and p16/p21-associated cellular senescence.
  3. Context-dependent pro-oxidant ROS accumulation in cancer cells, contributing to apoptosis, senescence, DNA damage, and chemosensitization.
  4. Suppression of proliferative and inflammatory survival signaling, including ↓NF-κB activity in susceptible cancer models.
  5. Suppression of cancer-cell invasion and metastatic phenotype in breast-cancer models.
  6. FEN1 downregulation and increased DNA-damage susceptibility, enhancing sensitivity to DNA-damaging chemotherapy such as paclitaxel in preclinical breast-cancer models.
  7. Antioxidant and cytoprotective activity in non-malignant tissues through polyphenol-mediated reduction of oxidative injury; this contrasts with the pro-oxidant response observed in some cancer models.

Bioavailability / PK relevance: Artichoke extract is a complex mixture rather than a single systemically delivered compound. Human pharmacokinetic studies demonstrate absorption and extensive metabolism of caffeoylquinic acids and flavonoids, with circulating metabolites such as caffeic/dihydrocaffeic-acid derivatives and conjugated flavonoids likely contributing to biological activity. Parent polyphenol exposure is relatively low and extensively transformed by intestinal, hepatic, and microbial metabolism. Extract composition and standardization are therefore major determinants of exposure.

In-vitro vs systemic exposure relevance: Many anticancer experiments use whole artichoke extracts at concentrations in the tens to hundreds of µg/mL range or prolonged cellular exposure. These conditions cannot be assumed to reproduce concentrations of intact extract constituents in human tumors after oral supplementation. Human circulating concentrations of individual absorbed polyphenols are generally in the submicromolar-to-low-micromolar range and are dominated by metabolites; consequently, direct extrapolation of cytotoxic in-vitro concentrations to oral systemic anticancer activity is not justified.

Clinical evidence status: Cancer: preclinical only; no established anticancer efficacy in humans and no validated role as cancer therapy or adjunct treatment. Non-cancer indications: multiple small randomized human trials and meta-analyses report effects on lipid parameters, and clinical studies have evaluated metabolic and hepatic outcomes. European herbal-medicine recognition is based principally on traditional use for dyspeptic gastrointestinal complaints rather than cancer treatment.

Safety / translation constraints: Artichoke leaf preparations are generally well tolerated in short-term human studies, but gastrointestinal adverse effects and allergic reactions can occur. Avoid in patients with hypersensitivity to artichoke or other Asteraceae plants. Because artichoke can stimulate bile secretion, bile-duct obstruction and cholangitis are important contraindications, and gallstones or other biliary disorders warrant medical assessment. Extract-to-extract chemical heterogeneity and the large exposure gap between many cell-culture experiments and oral human dosing are major constraints on anticancer translation.

Cancer-Relevant Mechanisms of Cynara scolymus Extract

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial apoptosis ↑ BAX, ↑ caspase-9, ↓ BCL-2, ↑ apoptosis ↔ / cytoprotective (context-dependent) R-G Programmed cancer-cell death Supported in oral squamous carcinoma and colorectal cancer models. Colon-cancer studies indicate activation of the mitochondrial-dependent apoptotic pathway.
2 Cell-cycle arrest and senescence ↑ G2/M arrest, ↑ p16, ↑ p21, ↑ senescence ↔ (model-dependent) G Suppression of proliferation G2/M arrest has been demonstrated in oral squamous carcinoma cells; prolonged low-dose exposure in MDA-MB-231 breast-cancer cells produces p16/p21-associated premature senescence.
3 ROS-mediated cancer stress ↑ ROS (dose-dependent), ↑ oxidative signaling ↓ oxidative stress P-G Apoptosis and senescence Artichoke polyphenols can behave as pro-oxidants in cancer cells while acting predominantly as antioxidants in non-malignant systems. NAC attenuation of growth inhibition supports a causal ROS component in breast-cancer models.
4 NF-κB and inflammatory survival signaling ↓ NF-κB, ↓ survival signaling ↓ excessive inflammatory signaling R-G Reduced proliferation and inflammation Artichoke leaf extract suppresses NF-κB activity in human leukemic-cell models, in part in association with AKR1B1 inhibition.
5 Invasion and metastatic phenotype ↓ invasion, ↓ metastatic phenotype ↔ G Reduced invasive behavior Polyphenolic artichoke extract reduces invasive potential in MDA-MB-231 breast-cancer cells. The precise molecular determinants appear extract- and model-dependent.
6 FEN1 and DNA damage response ↓ FEN1, ↑ DNA damage susceptibility Uncertain R-G Chemosensitization Artichoke polyphenols enhance chemotherapy response in breast-cancer cells through ROS-associated FEN1 downregulation and altered DNA-damage response.
7 Chemosensitization ↑ sensitivity to paclitaxel and DNA damage (model-dependent) Uncertain G Enhanced chemotherapy effect Observed preclinically with artichoke polyphenols plus paclitaxel; ROS/NRF2 and ERK signaling participate in the combination response. This has not been clinically validated.
8 NRF2 redox response ↕ NRF2 (context-dependent) ↑ antioxidant defense (context-dependent) P-R Redox adaptation NRF2 is involved in the ROS-dependent chemotherapy interaction described in breast-cancer cells but is not sufficiently consistent to classify as a universal primary anticancer mechanism of artichoke extract.
9 Antioxidant cytoprotection ↕ oxidative stress (context-dependent) ↓ ROS, ↓ oxidative injury, ↑ antioxidant capacity R-G Protection of non-malignant tissues Human and experimental non-cancer studies generally support antioxidant activity. This bidirectional redox behavior is important when interpreting apparently contradictory cancer and normal-tissue findings.
10 Clinical Translation Constraint In-vitro anticancer exposure often high Oral preparations generally well tolerated G Limits clinical inference Whole-extract concentrations used for cytotoxicity are not directly comparable with plasma exposure after oral ALE. Polyphenols undergo substantial metabolism, formulations vary chemically, and no clinical anticancer efficacy has been established.

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)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"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⟱
7429- CS,    Functional and Therapeutic Potential of Cynara scolymus in Health Benefits
- Review, Nor, NA - Review, IBD, NA - Review, AD, NA
*Inflam↓, *antiOx↑, *hepatoP↑, *lipid-P↓, *TNF-α↓, *ICAM-1↓, *IL1β↓, *IL6↓, *MUC1↑, *OCLN↑, *IBI↑, *ROS↓, *cardioP↑, *SOD↑, *GPx↑, *GSH↑, *TG/TAG↓, *LDL↓, *neuroP↑, *5HT↑, *BDNF↑,
7424- CS,  CGA,    Antioxidative and apoptotic properties of polyphenolic extracts from edible part of artichoke (Cynara scolymus L.) on cultured rat hepatocytes and on human hepatoma cells
- in-vitro, Nor, NA - in-vitro, Liver, HepG2
*ROS↓, *GSH↑, *MDA↓, tumCV↓, Apoptosis↑, Casp3↑,
7423- CS,    Prophylactic effects of Cynara scolymus L. leaf and flower hydroethanolic extracts against diethylnitrosamine/acetylaminoflourene-induced lung cancer in Wistar rats
- in-vivo, Nor, NA
*lipid-P↓, *GSTs↑, *GPx↑, *GSR↑, *SOD↑, *P53↑, *Bcl-2↑, *ROS↓,
7415- CS,    Artichoke Leaf Extract Inhibits AKR1B1 and Reduces NF-κB Activity in Human Leukemic Cells
- in-vitro, AML, THP1
AKR1B10↓, NF-kB↓, COX2/PTGS2↓, MMP2↓, ROS↓,
7411- CS,    Long Term Exposure to Polyphenols of Artichoke (Cynara scolymus L.) Exerts Induction of Senescence Driven Growth Arrest in the MDA-MB231 Human Breast Cancer Cell Line
- in-vitro, BC, MDA-MB-231 - in-vitro, CRC, HCT116
AntiCan↑, chemoPv↑, Apoptosis↑, TumCI↓, Casp↑, p16↑, P21↑, TumCCA↑, ROS↓, eff↓, TumCD↑, TumCG↓, cellSen↑, *ROS↓,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

AKR1B10↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 2,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 2,   Casp↑, 1,   Casp3↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

p16↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

TumCG↓, 1,  

Migration(tgid=13) ⓘ

MMP2↓, 1,   TumCI↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

cellSen↑, 1,   COX2/PTGS2↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoPv↑, 1,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   GPx↑, 2,   GSH↑, 2,   GSR↑, 1,   GSTs↑, 1,   lipid-P↓, 2,   MDA↓, 1,   ROS↓, 4,   SOD↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

LDL↓, 1,  

Cell Death(tgid=5) ⓘ

Bcl-2↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,  

Migration(tgid=13) ⓘ

MUC1↑, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,   OCLN↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ICAM-1↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   BDNF↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,   TG/TAG↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,  
Total Targets: 27

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
5 Cynara scolymus/Globe Artichoke/Artichoke Extract
1 Chlorogenic acid
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#:443  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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