Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry / ROS Cancer Research Results

Amla, Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry: Click to Expand ⟱
Features:

Phyllanthus emblica / Amla / Indian Gooseberry/Emblica officinalis — Phyllanthus emblica L. is the currently accepted botanical name for Amla or Indian Gooseberry; Emblica officinalis Gaertn. is a widely used botanical synonym commonly encountered in older pharmacological and Ayurvedic literature.

Type: Botanical extract / polyphenol-rich medicinal fruit

Active Constituents: Emblicanins, gallic acid, ellagic acid, tannins, flavonoids, vitamin C, and related polyphenolic compounds.

Function: Emblica officinalis extracts exhibit antioxidant, anti-inflammatory, metabolic, cytoprotective, and immunomodulatory activities. Experimental studies also demonstrate effects on apoptosis, proliferation, oxidative stress, inflammatory signaling, and mitochondrial function.

Cancer: Experimental studies report inhibition of tumor-cell proliferation, induction of apoptosis, suppression of inflammation and oxidative signaling, and modulation of pathways involved in invasion, angiogenesis, and tumor progression.

Alzheimer's Disease: Experimental neuroprotective evidence includes reduction of oxidative stress, neuroinflammation, mitochondrial dysfunction, and cognitive impairment in models relevant to neurodegeneration.

Triphala = ~⅓ Amla + ~⅓ Haritaki + ~⅓ Bibhitaki

Amla — Phyllanthus emblica L. is an edible medicinal fruit and polyphenol-rich botanical used in Ayurvedic medicine and as a food and natural health product. It is formally classified as a botanical food/nutraceutical and plant extract rather than an approved anticancer drug. Major constituents include hydrolysable tannins and ellagitannins such as emblicanins, punigluconin and related tannins, together with gallic acid, ellagic acid, flavonoids, quercetin derivatives and vitamin C. Extract composition varies substantially with cultivar, fruit processing and extraction method; therefore whole-fruit powder, aqueous extract and standardized polyphenol extracts should not be considered pharmacologically interchangeable.

Primary mechanisms (ranked):

  1. Antiproliferative and programmed-cell-death signaling, including Fas/death-receptor → caspase-8 → caspase-3/7 apoptosis in responsive cancer models.
  2. Autophagy induction through ↑ Beclin-1 and ↑ LC3B-II, particularly demonstrated in ovarian cancer cells and xenografts.
  3. Anti-angiogenic signaling with ↓ HIF-1α, ↓ tumor microvessel density and suppression of pro-angiogenic gene expression.
  4. Suppression of tumor invasion, migration and metastatic phenotypes, including inhibition of invasive breast-cancer-cell behavior.
  5. miR-375-mediated suppression of pro-angiogenic signaling in ovarian cancer models.
  6. Antioxidant and anti-inflammatory modulation, generally producing ↓ ROS/oxidative damage and ↓ NF-κB/AP-1-related inflammatory signaling in non-malignant or injury models; ROS direction in cancer cells is extract- and model-dependent and should not be treated as a universal pro-oxidant anticancer mechanism.
  7. Chemosensitization, including enhanced antiproliferative/autophagic effects with cisplatin in ovarian cancer models.
  8. Chemopreventive modulation of carcinogen-induced oxidative injury and carcinogen-metabolizing pathways in animal models.

Bioavailability / PK relevance: Oral amla is extensively transformed rather than circulating as an intact botanical extract. Ellagitannins and related polyphenols undergo gastrointestinal and microbiome metabolism, with urolithin conjugates among reported systemic metabolites. Human trials demonstrate biological activity after approximately 500–1000 mg/day standardized extracts, but there is no validated human pharmacokinetic exposure corresponding directly to the whole-extract concentrations used in cancer-cell experiments. Extract standardization and phytochemical composition are major translational variables.

In-vitro vs systemic exposure relevance: Many anticancer studies use approximately 25–300 µg/mL of whole amla extract. These concentrations cannot be directly equated with achievable plasma concentrations because the extract is a complex mixture whose tannins and polyphenols undergo extensive digestion, metabolism and conjugation. Accordingly, direct systemic reproduction of common in-vitro whole-extract exposure is unproven and likely overstates exposure to unchanged parent constituents. Xenograft and carcinogenesis studies provide stronger translational support than cell culture alone, but remain preclinical.

Clinical evidence status: Cancer evidence is preclinical. Antiproliferative, apoptotic, autophagic, anti-invasive and anti-angiogenic activity has been demonstrated in cultured cancer cells and several animal tumor models, but there is no established randomized clinical evidence showing that amla treats human cancer or improves cancer survival. Human RCTs exist for dyslipidemia, endothelial/metabolic endpoints and gastrointestinal disorders and provide useful safety information rather than anticancer efficacy. Amla is recognized by Health Canada as a natural health product ingredient and whole/minimally processed fruit has a history of safe food use; this does not constitute authorization as a cancer treatment.

Amla Cancer-Relevant Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells Primary Effect Notes / Interpretation
1 Fas death-receptor apoptosis ↑ Fas
↑ caspase-8
↑ caspase-3/7
↑ apoptosis		 ↔ or cytoprotective (context-dependent) Induction of programmed cancer-cell death Directly demonstrated with aqueous P. emblica extract in HeLa cells. Caspase-9 was not significantly activated in the principal study, supporting predominantly extrinsic rather than mitochondrial initiation.
2 Autophagy Beclin-1 LC3B ↑ Beclin-1
↑ LC3B-II
↑ autophagy		 Context-dependent Growth suppression through autophagic response Strongly demonstrated in ovarian cancer cells and mouse xenografts. In that model, amla suppressed proliferation without prominent apoptosis, illustrating cancer-type-dependent mechanism selection.
3 HIF-1α angiogenesis axis ↓ HIF-1α
↓ angiogenic genes
↓ CD31-positive vessels		 Not established Suppression of tumor angiogenesis Demonstrated in ovarian cancer cells and xenografts; one of the stronger in-vivo-supported anticancer mechanisms.
4 Cell proliferation and tumor growth ↓ proliferation
↓ clonogenic growth
↓ xenograft growth		 Relatively spared in selected models Direct growth inhibition Activity has been reported across lung, liver, cervical, breast, ovarian and colorectal cancer cell lines. Selectivity is incomplete but normal MRC5 fibroblasts and placental cells showed substantially less toxicity in individual studies.
5 Invasion and metastatic phenotype ↓ invasion
↓ migratory phenotype		 Not established Reduced invasive potential Aqueous extract inhibited MDA-MB-231 breast cancer cell invasion at lower concentrations than those used in several proliferation studies.
6 miR-375 pro-angiogenic signaling ↑ miR-375
↓ pro-angiogenic signaling		 Not established Epigenetic suppression of angiogenic signaling Reported in ovarian cancer cells and their exosomes; mechanistically useful but currently narrower in evidence base than HIF-1α suppression.
7 Cisplatin chemosensitization ↑ cisplatin antiproliferative effect
↑ autophagy		 Insufficient evidence Potential chemotherapy sensitization Synergistic activity was reported in ovarian cancer cells. This remains preclinical and should not be interpreted as evidence supporting clinical co-administration.
8 Inflammatory NF-κB AP-1 signaling ↓ inflammatory signaling (context-dependent) ↓ NF-κB
↓ AP-1
↓ inflammatory mediators		 Anti-inflammatory and cytoprotective modulation Mechanistically well supported in non-malignant oxidative-injury models. Direct causal importance to tumor killing is less established than apoptosis, autophagy or angiogenesis.
9 Oxidative stress and ROS ↔ / ↓ / occasionally ↑ downstream stress (model-dependent) ↓ ROS
↓ oxidative damage
↑ antioxidant defenses		 Redox modulation Amla should primarily be classified as an antioxidant botanical. Unlike Triphala, for which ROS-dependent cancer-cell killing has been demonstrated, isolated amla extract does not have sufficiently consistent evidence to assign universal ROS ↑ in cancer cells.
10 Carcinogenesis and tumor promotion ↓ tumor initiation/promotion
↓ tumor burden		 ↓ carcinogen-associated oxidative and tissue injury Chemoprevention Animal studies report reduced chemically induced tumor incidence, number and volume. These models support chemoprevention more strongly than treatment of established human cancer.
11 Clinical Translation Constraint Whole-extract concentrations commonly 25–300 µg/mL in vitro Human oral use generally tolerated in short-term studies Limits direct translation of experimental anticancer activity Extract heterogeneity, extensive polyphenol metabolism, uncertain tumor exposure, lack of oncology RCTs and absence of validated cancer dosing are the principal limitations.


Alzheimer's disease relevance: Amla has meaningful but exclusively preclinical neurodegeneration evidence. Tannoid principles of Emblica officinalis have improved cognition and attenuated biochemical and neuropathological abnormalities in experimental Alzheimer's-like models. Reported mechanisms include ↓ oxidative stress, ↓ neuroinflammation, protection of neuronal and mitochondrial function, modulation of tau-associated pathology and improvement of endogenous antioxidant defenses. More recent preclinical work also implicates autophagy and gut-microbiome modulation. There is no established clinical evidence that amla prevents or treats Alzheimer's disease in humans.

Clinical translation: The evidence supports retention of an AD section in the database, but it should be categorized as preclinical rather than clinical. Effects observed with purified tannoid fractions or polysaccharide fractions should not automatically be assigned quantitatively to generic amla fruit powder or commercial extracts.

Amla Alzheimer-Relevant Mechanisms

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Oxidative stress ↓ ROS-related oxidative injury
↓ lipid peroxidation
↑ antioxidant defenses		 Neuronal protection Among the most reproducible mechanisms in experimental neurodegeneration models.
2 Tau-associated pathology ↓ pathological tau-associated changes Reduced neurodegenerative pathology Reported particularly with isolated tannoid principles of E. officinalis in experimental AD/tau models.
3 Neuroinflammation ↓ inflammatory signaling Reduced neuronal inflammatory injury Likely overlaps with antioxidant and polyphenol-mediated signaling effects.
4 Mitochondrial function ↑ mitochondrial protection
↓ oxidative mitochondrial injury		 Improved neuronal bioenergetic resilience Predominantly preclinical evidence.
5 Autophagy ↑ autophagic regulation (model-dependent) Improved proteostasis and neuronal function Recent polysaccharide work associates cognitive improvement with autophagy modulation and microbiome changes.
6 Cognitive function ↑ learning
↑ memory		 Functional neuroprotection Observed in animal models; human AD efficacy has not been established.
7 Clinical Translation Constraint Preclinical evidence only Limits therapeutic inference No convincing human randomized trial demonstrating prevention or treatment of Alzheimer's disease.


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⟱
7397- Amla,    Clinical evaluation of Emblica Officinalis Gatertn (Amla) in healthy human subjects: Health benefits and safety results from a randomized, double-blind, crossover placebo-controlled study
- Trial, Nor, NA
*Dose↝, *other↑, *LDL↓, *HDL↑, *toxicity↑, *ROS↓,
7399- Amla,    Molecular Mechanisms of Cancer Prevention by Gooseberry (Phyllanthus emblica)
- Review, Var, NA
*Dose↝, *Inflam↓, *AntiCan↑, *antiOx↑, *neuroP↑, *hepatoP↑, *cardioP↑, *P450↓, *SOD↑, *GPx↑, *Catalase↑, *ROS↓, *CD4+↑, *CD19↑, *NK cell↑, Casp3↑, Casp7↑, Casp8↑, Casp9↑, Fas↑, BAX↑, Bcl-2↓, *IL10↑, *TNF-α↓, *IL6↓, *iNOS↓, *COX2/PTGS2↓, *GSTs↑, *NF-kB↓, *AP-1↓, *cJun↓, *lipid-P↓, TumCG↓, DNAdam↑, TumCCA↑, MMP2↓, MMP9↓,
7400- Amla,    Amla (Emblica officinalis Gaertn), a wonder berry in the treatment and prevention of cancer
- Review, Var, NA
radioP↑, ChemoSen↑, chemoPv↑, *ROS↓, antiOx↑, Inflam↓, Imm↑, *hepatoP↑, *cardioP↑, *lipid-P↓, TumCCA↑, Chk2↑, CDK1↓, CycB/CCNB1↓, CDC25↓, TumMeta↓,
7407- Amla,    Functional and Nutraceutical Significance of Amla (Phyllanthus emblica L.): A Review
- Review, Nor, NA
*Inflam↓, *antiOx↑, *GSH↑, *GPx↑, *SOD↑, *Catalase↑, *lipid-P↓, *ROS↓, *cardioP↑, *AntiDiabetic↑, *neuroP↑, *GastroP↑, *COX2/PTGS2↓, *MDA↓, *BAX↓, *TG/TAG↓, *HDL↑, *LDL↓, *HMG-CoA↓, *Dose↝, *CRP↓, DNAdam↑, Casp3↑, Casp7↑, Casp8↑, Fas↑, TumCI↓, selectivity↑,
7408- Amla,    Fresh Phyllanthus emblica (Amla) Fruit Supplementation Enhances Milk Fatty Acid Profiles and the Antioxidant Capacities of Milk and Blood in Dairy Cows
- Trial, Nor, NA
*Dose↝, *TAC↑, *SOD↑, *Albumin↑, *ROS↓, *other↑,
7409- Amla,    Clinical evaluation of Emblica Officinalis Gatertn (Amla) in healthy human subjects: Health benefits and safety results from a randomized, double-blind, crossover placebo-controlled study
- Trial, Nor, NA
*HDL↑, *LDL↓, *ROS↓, *AntiAg↑, *TBARS↓, *Dose↝,

Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 2,   Casp7↑, 2,   Casp8↑, 2,   Casp9↑, 1,   Chk2↑, 1,   Fas↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 2,  

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

TumCG↓, 1,  

Migration(tgid=13) ⓘ

MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumMeta↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Imm↑, 1,   Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   selectivity↑, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,   radioP↑, 1,  
Total Targets: 25

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

CD19↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 1,   GSTs↑, 1,   HDL↑, 3,   lipid-P↓, 3,   MDA↓, 1,   ROS↓, 6,   SOD↑, 3,   TAC↑, 1,   TBARS↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

HMG-CoA↓, 1,   LDL↓, 3,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,   other↑, 2,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,   AP-1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GastroP↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2/PTGS2↓, 2,   CRP↓, 1,   IL10↑, 1,   IL6↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   NK cell↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 5,   P450↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Albumin↑, 1,   CRP↓, 1,   IL6↓, 1,   TG/TAG↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 3,   hepatoP↑, 2,   neuroP↑, 2,   toxicity↑, 1,  
Total Targets: 43

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species
6 Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry
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#:442  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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