Bacopa monnieri / ROS Cancer Research Results

BM, Bacopa monnieri: Click to Expand ⟱
Features:

Bacopa monnieri — a medicinal botanical herb, also called Brahmi, typically used as a standardized oral extract enriched in bacosides, which are dammarane-type triterpenoid saponins. Its formal classification is a phytotherapeutic botanical / dietary supplement rather than an approved anticancer drug. Standard abbreviation: BM. The source is the aerial herb of Bacopa monnieri, a traditional Ayurvedic plant. Mechanistically, BM is best supported as a neurocognitive and cytoprotective adaptogenic extract; its anticancer activity is real but remains preclinical, heterogeneous, and often driven by isolated fractions or bacopasides rather than routine oral human exposure.

Primary mechanisms (ranked):

  1. Modulation of intrinsic apoptosis and cell-cycle arrest in cancer models
  2. Aquaporin-1 linked antitumor effects of bacopaside fractions, including reduced proliferation, migration, and angiogenic behavior
  3. Anti-inflammatory signaling with suppression of NF-κB-linked survival programs
  4. Context-dependent modulation of PI3K/AKT and MAPK stress-survival signaling
  5. Redox modulation: antioxidant / NRF2-linked cytoprotection in normal tissues, but possible pro-apoptotic oxidative stress at higher in-vitro tumor doses

Bioavailability / PK relevance: Oral BM extracts are usually standardized to bacosides, but bacosides have limited aqueous solubility and modest systemic exposure; in-vivo metabolism to aglycones / downstream metabolites likely matters. This creates a delivery constraint for oncology because many direct tumor effects are reported at micromolar in-vitro concentrations or with enriched fractions not clearly achievable after routine oral supplementation.

In-vitro vs systemic exposure relevance: Common anticancer in-vitro concentrations likely exceed typical oral systemic exposure. By contrast, cognition-related effects appear compatible with chronic low-level oral exposure and adaptive signaling over weeks rather than acute high plasma peaks.

Clinical evidence status: Small human RCT evidence exists for cognition / stress-related outcomes. Dementia / AD evidence remains inconclusive and low-certainty. Oncology evidence is preclinical only; there is no established clinical anticancer role.

Key Active Compounds
  Bacosides (especially bacoside A and B)
  Brahmin
  Hersaponin
  Betulinic acid
  Steroidal saponins

AD Pathways:
  ↓ Aβ accumulation
  ↓ Tau hyperphosphorylation
  ↓ Pro-inflammatory cytokines (e.g., IL-1β, TNF-α, IL-6)
  ↑ Acetylcholine levels	Inhibits AChE,
  Strong antioxidant activity	↓ ROS, ↑ SOD, ↑ catalase, and ↑ GSH levels.

Potential Anticancer Mechanisms
  Reduces oxidative stress
  Inhibits NF-κB and COX-2
  Anti-angiogenic
whole-extract Bacopa monnieri effects from purified bacopaside I / II mechanisms; this distinction matters because the more specific anticancer mechanisms are often fraction-specific.

Bacopa monnieri mechanistic pathway map

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Intrinsic apoptosis and cell-cycle control ↑ apoptosis; ↓ proliferation; G0/G1 or G2/M arrest (model-dependent) ↔ / cytoprotective R/G Tumor growth restraint Most reproducible cancer-facing effect across BM fractions and bacopasides; strength depends strongly on extract composition and concentration.
2 Aquaporin-1 axis ↓ proliferation; ↓ migration; ↓ invasion / angiogenic behavior ↔ R/G Membrane transport-linked antitumor effect This is one of the more specific mechanistic signals for bacopaside I / II, especially in colorectal and endothelial models; relevance is fraction-specific rather than clearly whole-extract universal.
3 NF-κB inflammatory survival signaling ↓ ↓ R/G Anti-inflammatory and anti-survival shift Likely contributes more confidently to normal-tissue neuroprotection than to a clinically useful direct anticancer effect.
4 PI3K/AKT and MAPK stress-survival signaling ↓ AKT; ERK/JNK/p38 modulation (context-dependent) ↔ / adaptive R/G Reduced survival signaling Reported in several models, but not yet a defining or standardized BM hallmark across tumor systems.
5 Mitochondrial ROS increase and apoptotic stress ↑ ROS (high concentration only); ↑ mitochondrial apoptosis ↓ oxidative injury P/R Redox bifurcation Important duality: normal tissues trend antioxidant, while some tumor models show pro-apoptotic oxidative stress only at higher exposures.
6 NRF2-linked antioxidant defense ↔ / ↑ (context-dependent) ↑ R/G Cytoprotection Central for neuroprotection and normal-cell antioxidant effects; in cancer this could be neutral or potentially counter-therapeutic depending on context, so it is not ranked as a core anticancer mechanism.
7 Angiogenesis and endothelial remodeling ↓ ↔ G Reduced vascular support Evidence is tied mainly to AQP1-active bacopaside work and endothelial assays rather than robust human translational data.
8 HIF-1α hypoxia adaptation ↓ (model-dependent) ↔ G Reduced hypoxic adaptation Secondary / contextual axis with limited direct evidence compared with apoptosis and AQP1-linked effects.
9 Chemosensitization or radiosensitization ↔ (insufficient evidence) ↔ G Not established No convincing clinical translation yet for use as a cancer sensitizer.
10 Clinical Translation Constraint ↓ ↓ — Exposure and standardization limitation Main constraints are extract heterogeneity, fraction-specific mechanisms, uncertain human tumor exposure, and lack of oncology trials.

TSF legend: P: 0–30 min
R: 30 min–3 hr
G: >3 hr



Bacopa monnieri (BM; Brahmi) — standardized extracts (typically 20–55% bacosides) studied in cognitive aging, MCI, and stress-related impairment. Mechanistically a neuroprotective adaptogen with antioxidant, anti-inflammatory, and synaptic plasticity–modulating effects.

Primary mechanisms (conceptual rank):
1) ↓ Oxidative stress (↑ NRF2-linked antioxidant enzymes; ↓ lipid peroxidation)
2) ↓ Neuroinflammation (↓ NF-κB; ↓ TNF-α / IL-1β in models)
3) ↑ Synaptic plasticity signaling (↑ BDNF/CREB; dendritic spine density in models)
4) ↓ Aβ aggregation / toxicity (preclinical emphasis)
5) Cholinergic modulation (↑ acetylcholine tone; acetylcholinesterase modulation)

Bioavailability / PK relevance: Orally bioavailable extracts cross the BBB at low concentrations; chronic dosing appears necessary for measurable cognitive benefit (weeks). Plasma levels modest; effects likely cumulative/adaptive rather than acute pharmacologic spikes.

Clinical evidence status: Multiple small RCTs show modest improvements in memory acquisition and processing speed in older adults and MCI; not disease-modifying approval for AD.

Bacopa monnieri — AD / Neurodegeneration Pathway Map

Rank Pathway / Axis Cells TSF Primary Effect Notes / Interpretation
1 ROS / Oxidative stress ↓ P/R Reduced neuronal oxidative burden Consistent antioxidant activity; decreases lipid peroxidation and improves endogenous antioxidant enzyme activity.
2 NRF2 axis ↑ R/G Stress-defense gene upregulation Supports increased SOD, catalase, glutathione enzymes; central to neuroprotection.
3 Neuroinflammation (NF-κB, cytokines) ↓ R/G Reduced microglial inflammatory signaling Important in slowing neurodegenerative progression in models.
4 BDNF / CREB signaling ↑ G Synaptic plasticity enhancement Linked to improved memory acquisition in animal and human cognitive studies.
5 Aβ aggregation / toxicity ↓ (preclinical) G Reduced amyloid-associated damage Shown in animal and cell models; human biomarker confirmation limited.
6 Cholinergic signaling ↑ tone (context-dependent) R/G Improved neurotransmission Modest acetylcholinesterase modulation and increased acetylcholine availability reported.
7 Mitochondrial function ↑ R/G Improved bioenergetic resilience Often secondary to reduced ROS and inflammation.
8 Ca²⁺ homeostasis ↔ / stabilized P/R Excitotoxic buffering Indirect stabilization through antioxidant and mitochondrial support.
9 Clinical Translation Constraint ↓ (constraint) — Modest effect size Benefits typically require ≥8–12 weeks; magnitude modest; not disease-modifying therapy.

TSF legend:
P: 0–30 min (direct antioxidant interactions)
R: 30 min–3 hr (acute signaling modulation)
G: >3 hr (gene regulation, synaptic adaptation)
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⟱
5483- BM,    The Role of Bacopa monnieri in Alzheimer’s Disease: Mechanisms and Potential Clinical Use—A Review
- Review, AD, NA
*cognitive↑, *neuroP↑, *PI3K↑, *Akt↑, *GSK‐3β↓, *tau↓, *ROS↓, *MMP3↓, *Casp1↓, *Casp3↓, *NF-kB↓, *TNF-α↓, *IL6↓,
3690- BM,    Neurocognitive Effect of Nootropic Drug Brahmi (Bacopa monnieri) in Alzheimer's Disease
- Review, AD, NA
*ROS↓, *5LO↓, *lipid-P↓, *GPx↑, *IronCh↑, *neuroP↑, *AChE↓, *memory↑, *toxicity↓, *SOD↑, *Catalase↑, *cognitive↑, *ChAT↑, *Ach↑, *BP↓,
5474- BM,    Pharmacological attributes of Bacopa monnieri extract: Current updates and clinical manifestation
*memory↑, *neuroP↑, *cognitive↑, *hepatoP↑, *antiOx↑, *AntiDiabetic↑, *fatigue↓, *GSK‐3β↓, *PI3K↑, *Akt↑, *tau↓, *ROS↓, *Inflam↓,
5473- BM,    Bacopa monnieri: Preclinical and Clinical Evidence of Neuroactive Effects, Safety of Use and the Search for Improved Bioavailability
- in-vivo, AD, NA - in-vivo, Park, NA
*neuroP↑, *toxicity∅, *AChE↓, *ROS↓, *antiOx↑, *lipid-P↓, *cognitive↑, *memory↑, *Dose↝, *BioAv↓, *TumCCA↑, *BBB↝,
3698- BM,    Bacopa monniera prevents from aluminium neurotoxicity in the cerebral cortex of rat brain
- in-vivo, AD, NA
*lipid-P↓, *ROS↓, *neuroP↑,
3697- BM,    Bacopa monnieri, a Neuroprotective Lead in Alzheimer Disease: A Review on Its Properties, Mechanisms of Action, and Preclinical and Clinical Studies
- Review, AD, NA
*ROS↓, *cognitive↑, *memory↑, *BBB↑, *P-gp↓, *CYP3A2↓,
3695- BM,    Bacopa monnieri (L.) wettst. Extract protects against glutamate toxicity and increases the longevity of Caenorhabditis elegans
- in-vitro, AD, HT22
*OS↑, *mt-ROS↓, *ROS↓, *neuroP↑, *ER Stress↓,
3693- BM,    Bacopa monnieri prevents colchicine-induced dementia by anti-inflammatory action
- in-vivo, AD, NA
*cognitive↑, *Aβ↓, *BACE↓, *Inflam↓, *ROS↓, *antiOx↑,
3692- BM,    Brahmi (Bacopa monnieri): An ayurvedic herb against the Alzheimer's disease
- Review, AD, NA
*neuroP↑, *ROS↓, *Inflam↓, *Aβ↓, *cognitive↑,

Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 1,   GPx↑, 1,   lipid-P↓, 3,   ROS↓, 9,   mt-ROS↓, 1,   SOD↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Core Metabolism/Glycolysis ⓘ

CYP3A2↓, 1,  

Cell Death ⓘ

Akt↑, 2,   Casp1↓, 1,   Casp3↓, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 2,   PI3K↑, 2,  

Migration ⓘ

5LO↓, 1,   MMP3↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   BBB↝, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   Inflam↓, 3,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,   ChAT↑, 1,   tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   Dose↝, 1,  

Clinical Biomarkers ⓘ

BP↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cognitive↑, 7,   fatigue↓, 1,   hepatoP↑, 1,   memory↑, 4,   neuroP↑, 7,   OS↑, 1,   toxicity↓, 1,   toxicity∅, 1,  
Total Targets: 44

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
9 Bacopa monnieri
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#:339  Target#:275  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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