VitC Cancer Research Results

VitC, Vitamin C levels: Click to Expand ⟱
Source:
Type:
Adequate intracellular vitamin C can contribute to the hydroxylation and subsequent degradation of HIF-1α. Elevated HIF-1α is often associated with aggressive tumor behavior and poor prognosis.

Ascorbate Transporters
• SVCT2 (Sodium-Dependent Vitamin C Transporter 2)
– Role: Mediates the uptake of ascorbate into cells.
• GLUT Transporters (e.g., GLUT1)
– Role: While primarily known for transporting glucose, certain GLUT family members (especially GLUT1) also facilitate the uptake of the oxidized form of vitamin C (dehydroascorbate).
Ascorbic acid is a water-soluble redox-active molecule with three core roles relevant to cancer:
-Antioxidant / redox buffer (scavenges ROS)
-Cofactor for dioxygenases
  -TET DNA demethylases
  -JmjC histone demethylases
-Pro-oxidant at high pharmacologic concentrations (via H₂O₂ generation)

Its biological impact depends on dose, route, and tumor redox state.
Dose & Route Matter 
-Physiologic AA (oral): antioxidant, homeostatic
-Pharmacologic AA (IV, millimolar plasma levels):
  -Can act as a pro-oxidant in tumors
  -Generates extracellular H₂O₂ selectively toxic to some cancers

This is therapeutic context, not biomarker use—but it explains why AA status matters.



Scientific Papers found: Click to Expand⟱
3972- ACNs,    Recent Research on the Health Benefits of Blueberries and Their Anthocyanins
- Review, AD, NA - Review, Park, NA
*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.

3542- ALA,    Chelation: Harnessing and Enhancing Heavy Metal Detoxification—A Review
- Review, Var, NA
*antiOx↑, powerful antioxidant that regenerates other antioxidants (e.g., vitamins E and C, and reduced glutathione) and has metal-chelating activity.
*VitE↑,
*VitC↑,
*GSH↑,
*IronCh↑,
*BioAv↑, Both fat and water soluble, it is readily absorbed from the gut and crosses cellular and blood-brain membrane barriers
*BBB↑,

3547- ALA,    Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration
- Review, AD, NA - Review, Park, NA
*memory↑, a number of preclinical studies showing beneficial effects of LA in memory functioning, and pointing to its neuroprotective potential effect
*neuroP↑,
*motorD↑, Improved motor dysfunction
*VitC↑, elevates the activities of antioxidants such as ascorbate (vitamin C), α-tocoferol (vitamin E) (Arivazhagan and Panneerselvam, 2000), glutathione (GSH)
*VitE↑,
*GSH↑,
*SOD↑, superoxide dismutase (SOD) activity (Arivazhagan et al., 2002; Cui et al., 2006; Militao et al., 2010), catalase (CAT) (Arivazhagan et al., 2002; Militao et al., 2010), glutathione peroxidase (GSH-Px)
*Catalase↑,
*GPx↑,
*5HT↑, ↑levels of neurotransmitters (dopamine, serotonin and norepinephrine) in various brain regions
*lipid-P↓, ↓ level of lipid peroxidation,
*IronCh↑, ↓cerebral iron levels,
*AChE↓, ↓ AChE activity, ↓ inflammation
*Inflam↓,
*GlucoseCon↑, ↑brain glucose uptake; ↑ in the total GLUT3 and GLUT4 in the old mice;
*GLUT3↑,
*GLUT4↑,
NF-kB↓, authors showed that LA inhibited the stimulation of nuclear factor-κB (NF-κB)
*IGF-1↑, LA restored the parameters of total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interlukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Mahboob et al. (2016), analyzed the effects of LA in AlCl3- model of neurodegeneration,
*IL1β↓,
*TNF-α↓, Suppression of NF-κβ p65 translocation and production of proinflammatory cytokines (IL-6 and TNF-α) followed inhibition of cleaved caspase-3
*cognitive↑, demonstrating its capacity in ameliorating cognitive functions and enhancing cholinergic system functions
*ChAT↑, LA treatment increased the expression of muscarinic receptor genes M1, M2 and choline acetyltransferase (ChaT) relative to AlCl3-treated group.
*HO-1↑, R-LA and S-LA also enhanced expression of genes related to anti-oxidative response such as heme oxygenase-1 (HO-1) and phase II detoxification enzymes such as NAD(P)H:Quinone Oxidoreductase 1 (NQO1).
*NQO1↑,

3545- ALA,    Potential therapeutic effects of alpha lipoic acid in memory disorders
- Review, AD, NA
*neuroP↑, potential therapeutic effects for the prevention or treatment of neurodegenerative disease
*Inflam↓, ALA is able to regulate inflammatory cell infiltration into the central nervous system and to down-regulate VCAM-1 and human monocyte adhesion to epithelial cells
*VCAM-1↓, down-regulate vascular cell adhesion molecule-1 (VCAM-1) and the human monocyte adhesion to epithelial cells
*5HT↑, ALA is able to improve the function of the dopamine, serotonin and norepinephrine neurotransmitters
*memory↑, scientific evidence shows that ALA possesses the ability to improve memory capacity in a number of experimental neurodegenerative disease models and in age-related cognitive decline in rodents
*BioAv↝, Between 27 and 34% of the oral intake is available for tissue absorption; the liver is one of the main clearance organs on account of its high absorption and storage capacity
*Half-Life↓, The plasma half-life of ALA is approximately 30 minutes. Peak urinary excretion occurs 3-6 hours after intake.
*NF-kB↓, As an inhibitor of NF-κβ, ALA has been studied in cytokine-mediated inflammation
*antiOx↑, In addition to the direct antioxidant properties of ALA, some studies have shown that both ALA and DHLA and a great capacity to chelate redox-active metals, such as copper, free iron, zinc and magnesium, albeit in different ways (
*IronCh↑, ALA is able to chelate transition metal ions and, therefore, modulate the iron- and copper-mediated oxidative stress in Alzheimer’s plaques
*ROS↓, iron and copper chelation with DHLA may explain the low level of free radical damage in the brain and the improvement in the pathobiology of Alzheimer’s Disease
*ATP↑, ALA may increase the mitochondrial synthesis of ATP in the brain of elderly rats, thereby increasing the activity of the mitochondrial enzymes
*ChAT↑, ALA may also play a role in the activation of the choline acetyltransferase enzyme (ChAT), which is essential in the anabolism of acetylcholine
*Ach↑,
*cognitive↑, One experimental study has shown that in rats that had been administered ALA there was an inversion in the cognitive dysfunction with an increase in ChAT activity in the hippocampus
*lipid-P↓, administration of ALA reduces lipid peroxidation in different areas of the brain and increases the activity of antioxidants such as ascorbate (vitamin C), α-tocopherol (vitamin E), glutathione,
*VitC↑,
*VitE↑,
*GSH↑,
*SOD↑, and also the activity of superoxide dismutase, catalase, glutathione-peroxidase, glutathione-reductase, glucose-6-P-dehydrogenase
*Catalase↑,
*GPx↑,
*Aβ↓, Both ALA and DHLA have been seen to inhibit the formation of Aβ fibrils

3544- ALA,    Alpha lipoic acid for dementia
- Review, AD, NA
*antiOx↑, ALA is a low molecular weight antioxidant, readily absorbed from the diet or an oral dose, and crosses the blood brain barrier
*BBB↑,
*VitC↑, DHLA regenerates through redox cycling other antioxidants like vitamin C and E and raises levels of intracellular glutathione, an important thiol antioxidant
*VitE↑,
*GSH↑,
*IronCh↑, ALA al- so chelates certain metals, forming stable complexes with copper, manganese and zinc (Sigel 1978)
*neuroP↑, ALA would seem an ideal candidate as an antioxidant agent in neurodegenerative diseases.
*NO↓, ALA also modulates nitric oxide levels in brain and neural tissue, which may have effects in neurodegeneration, learning, cognition, and aging (Gross 1995)
*cognitive↑, elderly patients with dementia were given ALA. Findings suggested a stabilization of cognitive functions in the study group,
*AntiAge↑,
*memory↑, ALA has gained considerable attention following studies demonstrating partial reversal of memory loss in aged rats.
*ROS↓, scavenging hy- droxyl or superoxide radicals (Suzuki 1991) and by scavenging per- oxyl radicals (

7402- Amla,    Traditional knowledge to clinical trials: A review on therapeutic actions of Emblica officinalis
- Review, Var, NA
*eff↑, E.officinalis is one of the major component in various health tonics, also exerts synergistic effects in enhancing the medicinal efficacy.
*antiOx↑, antioxidant, anticancer, immunomodulator, anti-inflammatory, cyto-protective properties
*AntiCan↑,
*Imm↑,
*Inflam↓, In trial phase I, oral doses of 3 capsules per day for two weeks showed significant immuno-stimulatory effects on cytotoxic T cells and natural killer cells.
*AntiArt↑, The present review analysed and summarized the pharmacological actions, experimental studies and clinical trials of E. officinalis with emphasis on its immuno-enhancer, antiinflammatory and anticancer activities
*Dose↝, The fruit of amla consists of many bioactive compounds including ellagic acid, chebulinic acid, apigenin, gallic acid, quercetin, chebulagic acid, isostrictiniin, corilagin, methyl gallate, luteolin etc
*VitC↑, It has been reported that 100 g of edible fruit provides 470–680 mg of Vit. C.
radioP↑, figure 1
*cardioP↑,
*GastroP↑,
*Wound Healing↑,
*Diar↓,
eff↑, They reported that IC50 of Amla alone and PE-AgNP were 30 mg/mL and 20 mg/mL respectively, while these nanoparticles demonstrated potential antiproliferative effect by oxidative stress, mitochondrial depolar ization, DNA damage and apoptotic functio
NK cell↑, Enhanced natural killer (NK) cell activity and antibody dependent cellular cytotoxicity
BAX↑, Up-regulation of Bax expression and down-regulation of Bcl-2 expression.Cell cycle arres
Bcl-2↓,
TumCCA↑,
Dose↝, Powdered amla fruit at dosage of 1, 2 or 3 g orally given with 30 ml water once daily in the morning after breakfast for 21 days

3673- Ash,    An overview on ashwagandha: a Rasayana (rejuvenator) of Ayurveda
- Review, NA, NA
*cognitive↑, Cognition Promoting Effect
*Inflam↓, anti-inflammatory and anti-arthritic
*Strength↑, swimming time was approximately doubled after Withania somnifera (WS) treatment
*VitC↑, Withania somnifera treatment prevents, decrease of adrenal cortisol and ascorbic acid which occurs due to swimming stress.
*memory↑, It is useful for different types of diseases like Parkinson, dementia, memory loss, stress induced diseases, malignoma and others.

2794- CHr,    An updated review on the versatile role of chrysin in neurological diseases: Chemistry, pharmacology, and drug delivery approaches
- Review, Park, NA - Review, Stroke, NA
*neuroP↑, chrysin has protective effects against neurological conditions by modulating oxidative stress, inflammation, and apoptosis in animal models.
*ROS↓,
*Inflam↓,
*Apoptosis↓,
*IL1β↓, attenuated IL-1β and TNF-α, COX-2, iNOS, and NF-kB expression, activated JNK
*TNF-α↓,
*COX2/PTGS2↓,
*iNOS↓,
*NF-kB↓,
*JNK↓,
*HDAC↓, alleviated histone deacetylase (HDCA) activity, GSK-3β levels, IFNγ, IL-17,
*GSK‐3β↓,
*IFN-γ↓,
*IL17↓,
*GSH↑, increased GSH levels
*NRF2↑, Park's: Increased Nrf2, modulated HO-1, SOD, CAT, decreased MDA, inhibited NF-κB and iNOS
*HO-1↑, upregulated expression of hallmark antioxidant enzymes, including HO-1, SOD, and CAT; and decreased levels of MDA
*SOD↑,
*MDA↓,
*NO↓, Attenuated NO, increased GPx
*GPx↑,
*TBARS↓, decreased levels of TBARS, AChE, restored activities of GR, GSH, SOD, CAT and Vitamin C
*AChE↓,
*GR↑,
*Catalase↑,
*VitC↑,
*memory↑, attenuated memory impairment
*lipid-P↓, attenuated lipid peroxidation
*ROS↓, attenuated ROS

7436- Chy,  Amla,    A Review on the Role of Amla and Chyawanprash in Immunity Enhancement and Disease Prevention
*VitC↑, hyawanprash is formulated by processing around 50 medicinal herbs and their extracts, including the prime ingredient, Amla (Indian gooseberry), which is the world’s richest source of vitamin C.
*memory↑, Chyawanprash has been used to help strengthen your digestive system and promote food absorption, corrects hyperacidity, dyspepsia and flatulence, peptic ulcers and gastritis, boost memory power, promote cardio fitness by supporting your heart and hel
*Imm↑, demonstrated immune-enhancing properties, with traditional preparations like Chyawanprash showing immunostimulatory effects, including enhanced natural killer (NK) cell activity and cytokine release in clinical studies.
*NK cell↑,
*antiOx↑, Modern research shows antioxidant, adaptogenic, and neuroprotective properties that support cognitive function and mental resilience
*neuroP↑,
*cognitive↑,

4025- FulvicA,    Mumio (Shilajit) as a potential chemotherapeutic for the urinary bladder cancer treatment
- in-vitro, Bladder, T24/HTB-9 - Review, AD, NA
tumCV↓, Mumio affected the viability of both cell types in a time and concentration dependent manner
selectivity↑, We observed a selectivity of Mumio against cancer cells. Our results showed that Mumio was significantly more cytotoxic to urinary bladder cancer cells than to normal cells.
TumCCA↑, Cell cycle and apoptosis analysis showed that Mumio inhibited G0/G1 or S phase cell cycle, which in turn induced apoptosis.
other↝, Different names are used depending on where it is found such as: Mumijo, Mumie (Russia), Saljit, Shilajit (India), Kao-Tun (Birma), Arakul Dshabal (Kyrgyzstan) and many others
*neuroP↑, Mumio is considered to improve memory and to inhibit aging of the brain through its neuroprotective activity
*memory↑,
*tau↓, mechanism of action is based on fulvic acid-mediated prevention of Tau self-aggregation
*other↝, ain components of Mumio are humus (60–80%), benzoic acid, fatty acids, ichthyol, ellagic acid, resin, triterpenes, sterol, aromatic carboxylic acids, bioactive 3,4-benzokoumarins, amino acids, phenolic lipids and microelements.
*lipid-P↓, Ghosal et al. showed that these acids inhibit lipid peroxidation and possess the ability to recycle ascorbic acid and thereby exhibiting significant antioxidant activity
*VitC↑,
*antiOx↑,

7543- HT,    Hydroxytyrosol supplementation increases vitamin C levels in vivo. A human volunteer trial
- Trial, Nor, NA
VitC↑, vitamin C increased by two-fold at T4 and T8 compared with levels at baseline.

7848- ISQ,    Review of anticancer mechanisms of isoquercitin
- Review, Var, NA
BioAv↑, This compound presents similar therapeutic profiles to quercetin but with superior bioavailability, resulting in increased efficacy compared to the aglycone form.
eff↑,
*antiOx↓, pharmacological effects including antioxidant, antiproliferative, anti-inflammatory, anti-hypertensive, and anti-diabetic.
TumCP↓,
*Inflam↓,
*AntiDiabetic↑,
lipid-P↓, The protective effects of IQ in cancer may be due to actions on lipid peroxidation.
*toxicity↓, Flavonoids are a group of polyphenolic compounds and as a part of the human diet, they have very low toxicity in addition to various beneficial health effects
*Half-Life↝, Human "Juice mix" Quercitin - 216 ± 96 mins
*Half-Life↑, Human Shallot flesh Isoquercitin 15 13980 ± 30
*XO↝, IQ exerts antioxidative effects by inhibiting lipid peroxidation via interference with enzyme activity (xanthine oxidase), chelation of redox-active metals, increased absorption of vitamin C, and direct scavenging of ROS
*IronCh↝,
*VitC↑,
*ROS↓,
β-catenin/ZEB1↓, IQ for example, acts directly by inhibiting the nuclear translocation of β-catenin protein and exhibits significant anti-proliferative effects on glioblastoma cells
Casp3↑, IQ activated caspase-3, 8, and 9 and reduced the mitochondrial membrane potential.
Casp8↑,
Casp9↑,
MMP↓,
p‑ERK↓, IQ inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) and promoted the phosphorylation of c-Jun N-terminal kinase (JuNK).
p‑cJun↑,

3528- Lyco,    The Importance of Antioxidant Activity for the Health-Promoting Effect of Lycopene
- Review, Nor, NA - Review, AD, NA - Review, Park, NA
*antiOx↑, the antioxidant effect of lycopene
*ROS↓, Lycopene has the ability to reduce reactive oxygen species (ROS) and eliminate singlet oxygen, nitrogen dioxide, hydroxyl radicals, and hydrogen peroxide
*BioAv↝, human body cannot synthesize lycopene. It must be supplied with the diet
*Half-Life↑, half-life of lycopene in human plasma is 12–33 days
*BioAv↓, bioavailability decreases with age and in the case of certain diseases
*BioAv↑, heat treatment process of food increases the bioavailability of lycopene
*cardioP↑, positive effect on cardiovascular diseases, including the regulation of blood lipid levels
*neuroP↑, beneficial effects in nervous system disorders, including neurodegenerative diseases such as Parkinson′s disease and Alzheimer′s disease
*H2O2↓, Lycopene has the ability to reduce reactive oxygen species (ROS) and eliminate singlet oxygen, nitrogen dioxide, hydroxyl radicals, and hydrogen peroxide
*VitC↑, ability to regenerate non-enzymatic antioxidants such as vitamin C and E.
*VitE↑,
*GPx↑, increase in cardiac GSH-Px activity and an increase in cardiac GSH levels
*GSH↑,
*MPO↓, also a decrease in the level of cardiac myeloperoxidase (MPO), cardiac H2O2, and a decrease in cardiac glutathione S transferase (GSH-ST) activity.
*GSTs↓,
*SOD↑, increasing the activity of GSH-Px and SOD in the liver
*NF-kB↓, reducing the expression of NF-κB mRNA in the heart
*IL1β↓, decreased the level of IL-1β and IL-6 and increased the level of anti-inflammatory IL-10 in the heart
*IL6↓,
*IL10↑,
*MAPK↓, inhibited the activation of the ROS-dependent pro-hypertrophic mitogen-activated protein kinase (MAPK) and protein kinase B (Akt) signaling pathways.
*Akt↓,
*COX2/PTGS2↓, decrease in the levels of pro-inflammatory mediators in heart: COX-2, TNF-α, IL-6, and IL-1β and an increase in the anti-inflammatory cardiac TGF-β1.
*TNF-α↓,
*TGF-β1↑,
*NO↓, reduced NO levels in heart and cardiac NOS activity
*GSR↑, increase in the level of cardiac and hepatic SOD, CAT, GSH, GPx, and glutathione reductase (GR)
*NRF2↑, It also activated nuclear factor-erythroid 2 related factor 2 (Nrf2). This affected the downstream expression of HO-1 [97].
*HO-1↑,
*TAC↑, Researchers observed an increase in the liver in TAC and GSH levels and an increase in GSH-Px and SOD activity
*Inflam↓, study showed that lycopene was anti-inflammatory
*BBB↑, Lycopene is a lipophilic compound, which makes it easier to penetrate the blood–brain barrier.
*neuroP↑, Lycopene had also a neuroprotective effect by restoring the balance of the NF-κB/Nrf2 pathway.
*memory↑, lycopene on LPS-induced neuroinflammation and oxidative stress in C57BL/6J mice. The tested carotenoid prevented memory loss

3001- RosA,    Therapeutic Potential of Rosmarinic Acid: A Comprehensive Review
- Review, Var, NA
TumCP↓, including in tumor cell proliferation, apoptosis, metastasis, and inflammation
Apoptosis↑,
TumMeta↓,
Inflam↓,
*antiOx↑, RA is therefore considered to be the strongest antioxidant of all hydroxycinnamic acid derivatives
*AntiAge↑, , it also exerts powerful antimicrobial, anti-inflammatory, antioxidant and even antidepressant, anti-aging effects
*ROS↓, RA and its metabolites can directly neutralize reactive oxygen species (ROS) [10] and thereby reduce the formation of oxidative damage products.
BioAv↑, RA is water-soluble, and according to literature data, the efficacy of secretion of this compound in infusions is about 90%
Dose↝, Accordingly, it is possible to consume approximately 110 mg RA daily, i.e., approximately 1.6 mg/kg for adult men weighing 70 kg.
NRF2↑, liver cancer cell line, HepG2, transfected with plasmid containing ARE-luciferin gene, RA predominantly enhances ARE-luciferin activity and promotes nuclear factor E2-related factor-2 (Nrf2) translocation from cytoplasm to the nucleus
P-gp/ABCB1↑, and also increases MRP2 and P-gp efflux activity along with intercellular ATP level
ATP↑,
MMPs↓, RA concurrently induced necrosis and apoptosis and stimulated MMP dysfunction activated PARP-cleavage and caspase-independent apoptosis.
cl‑PARP↓,
Hif1a↓, inhibits transcription factor hypoxia-inducible factor-1α (HIF-1α) expression
GlucoseCon↓, it also suppressed glucose consumption and lactate production in colorectal cells
lactateProd↓,
Warburg↓, may suppress the Warburg effects through an inflammatory pathway involving activator of transcription-3 (STAT3) and signal transducer of interleukin (IL)-6
TNF-α↓, RA supplementation also reduced tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2) and IL-6 levels, and modulated p65 expression [
COX2/PTGS2↓,
IL6↓,
HDAC2↓, RA induced the cell cycle arrest and apoptosis in prostate cancer cell lines (PCa, PC-3, and DU145) [31]. These effects were mediated through modulation of histone deacetylases expression (HDACs), specifically HDAC2;
GSH↑, RA can also inhibit adhesion, invasion, and migration of Ls 174-T human colon carcinoma cells through enhancing GSH levels and decreasing ROS levels
ROS↓,
ChemoSen↑, RA also enhances chemosensitivity of human resistant gastric carcinoma SGC7901 cells
*BG↓, RA significantly increased insulin index sensitivity and reduced blood glucose, advanced glycation end-products, HbA1c, IL-1β, TNFα, IL-6, p-JNK, P38 mitogen-activated protein kinase (MAPK), and NF-κB levels
*IL1β↓,
*TNF-α↓,
*IL6↓,
*p‑JNK↓,
*p38↓,
*Catalase↑, The reduced activities of CAT, SOD, glutathione S-transferases (GST), and glutathione peroxidase (GPx) and the reduced levels of vitamins C and E, ceruloplasmin, and GSH in plasma of diabetic rats were also significantly recovered by RA application
*SOD↑,
*GSTs↑,
*VitC↑,
*VitE↑,
*GSH↑,
*GutMicro↑, protective effects of RA (30 mg/kg) against hypoglycemia, hyperlipidemia, oxidative stress, and an imbalanced gut microbiota architecture was studied in diabetic rats.
*cardioP↑, Cardioprotective Activity: RA also reduced fasting serum levels of vascular cell adhesion molecule 1 (VCAM-1), inter-cellular adhesion molecule 1 (ICAM-1), plasminogen-activator-inhibitor-1 (PAI-1), and increased GPX and SOD levels
*ROS↓, Finally, in H9c2 cardiac muscle cells, RA inhibited apoptosis by decreasing intracellular ROS generation and recovering mitochondria membrane potential
*MMP↓,
*lipid-P↓, At once, RA suppresses lipid peroxidation (LPO) and ROS generation, whereas in HSC-T6 cells it increases cellular GSH.
*NRF2↑, Additionally, it significantly increases Nrf2 translocation
*hepatoP↑, Hepatoprotective Activity
*neuroP↑, Nephroprotective Activity
*P450↑, RA also reduced CP-produced oxidative stress and amplified cytochrome P450 2E1 (CYP2E1), HO-1, and renal-4-hydroxynonenal expression.
*HO-1↑,
*AntiAge↑, Anti-Aging Activity
*motorD↓, A significantly delays motor neuron dysfunction in paw grip endurance tests,

4488- Se,  Chit,  PEG,    Anticancer effect of selenium/chitosan/polyethylene glycol/allyl isothiocyanate nanocomposites against diethylnitrosamine-induced liver cancer in rats
- in-vivo, Liver, HepG2 - in-vivo, Nor, HL7702
tumCV↓, The SCPg-AI-NCs effectively decreased the cell viability and induced apoptosis in the HepG2 cells.
Apoptosis↑,
*GSH↑, The SCPg-AI-NCs treatment effectively decreased the TBARS and improved the GSH, vitamin-C & -E contents in the DEN-induced rats
*VitC↑,
*VitE↑,
*SOD↑, The activities of SOD, GPx, and GR were also improved by the SCPg-AI-NCs treatment in the DEN-induced rats.
*GPx↑,
*GR↑,
ALAT↓, The activities of ALT, ALP, AST, LDH, and GGT was remarkably decreased by the SCPg-AI-NCs treatment in the DEN-provoked liver cancer rats.
ALP↓,
AST↓,
LDH↓,
selectivity↑, same doses of SCPg-AI-NCs did not showed the cytotoxicity to the normal liver HL7702 cells
eff↑, The utilization of nanocomposites as drug delivery systems has a efficacy to solve the several side effects triggered by chemotherapeutic drugs to normal cells

3655- SIL,    Protective effect of silymarin on oxidative stress in rat brain
- in-vivo, AD, NA
*GSH↑, After SM administration GSH and AA significantly increase and SOD activity was significantly enhanced
*VitC↑,
*SOD↑,
*lipid-P↓, SM may to protect the SNC by oxidative damage for its ability to prevent lipid peroxidation and replenishing the GSH levels.
*ROS↓,
*hepatoP↑, Silybum marianum (L.) Gaertn., known as milk thistle, is one of the most popular herbal remedies for liver disease.
*neuroP↑, small number of reports of the SM effects on brain, concerning protective effect on fetal rat brain by ethanol induced injury

2134- TQ,    Modulation of Nrf2/HO1 Pathway by Thymoquinone to Exert Protection Against Diazinon-induced Myocardial Infarction in Rats
- in-vivo, Nor, NA
*ALAT↓, CK-MB, ALT, and AST) were shown. DN-treated rats showed significantly elevated enzyme activities as compared with control rats (147.33 ± 20.85, 110.67 ± 9.65, and 407.5 ± 31.3, respectively), and these abnormalities were alleviated in the TQ treatmen
*AST↓,
*MDA↓, TQ treatment to DN intoxicated rats significantly decreased MDA levels when compared with the DN alone group of rats, recommending the protective antioxidant role of TQ
*ROS↓,
*GSSG↓, GSSG that exhibit significant elevation in DN intoxication and normalized levels during TQ treatment.
*GSH↑, Administration of TQ with DN during the experimental period significantly increased GSH (heart and serum), vit-E and vit-C contents to near normal levels in the heart tissues and serum
*VitE↑,
*VitC↑,
*NRF2↑, TQ, significantly increased Nrf2, HO-1, NQO1, and SOD were noticed (22.2 ± 1.41, 37.2 ± 2.6, 33.37 ± 4.28, and 52.7 ± 3.05, respectively), when compared to the DN intoxicated group.
*HO-1↑,
*NQO1↑,
*SOD↑,
*cardioP↑, Restoration of body weight and improvement in heart weight in TQ treatment showed beneficial effects of TQ treatment.
*GSH/GSSG↑, TQ has a significant efficacy to control the levels of oxidized and reduced glutathione pools and able to decrease the GSSG/GSH ratio.
*GPx↑, TQ enhances GSH and GPx activities in DN-intoxicated rats by a beneficial mechanism.


Showing Research Papers: 1 to 17 of 17

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 17

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1)

GSH↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 1,   VitC↑, 1,  

Mitochondria & Bioenergetics(tgid=3)

ATP↑, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

ALAT↓, 1,   GlucoseCon↓, 1,   lactateProd↓, 1,   LDH↓, 1,   Warburg↓, 1,  

Cell Death(tgid=5)

Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,  

Transcription & Epigenetics(tgid=7)

p‑cJun↑, 1,   other↝, 1,   tumCV↓, 2,  

DNA Damage & Repair(tgid=10)

cl‑PARP↓, 1,  

Cell Cycle & Senescence(tgid=11)

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12)

p‑ERK↓, 1,   HDAC2↓, 1,  

Migration(tgid=13)

MMPs↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14)

Hif1a↓, 1,  

Barriers & Transport(tgid=15)

P-gp/ABCB1↑, 1,  

Immune & Inflammatory Signaling(tgid=16)

COX2/PTGS2↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   NK cell↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↑, 2,   ChemoSen↑, 1,   Dose↝, 2,   eff↑, 3,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22)

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   IL6↓, 1,   LDH↓, 1,  

Functional Outcomes(tgid=23)

radioP↑, 1,  
Total Targets: 48

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0)

AntiArt↑, 1,  

Redox & Oxidative Stress(tgid=1)

antiOx↓, 2,   antiOx↑, 8,   Catalase↑, 4,   GPx↑, 7,   GSH↑, 11,   GSH/GSSG↑, 1,   GSR↑, 1,   GSSG↓, 1,   GSTs↓, 1,   GSTs↑, 1,   H2O2↓, 1,   HDL↑, 1,   HO-1↑, 5,   lipid-P↓, 6,   MDA↓, 3,   MPO↓, 1,   NQO1↑, 2,   NRF2↑, 4,   ROS↓, 10,   SOD↑, 9,   TAC↑, 1,   TBARS↓, 1,   VitC↑, 16,   VitE↑, 8,  

Metal & Cofactor Biology(tgid=2)

IronCh↑, 4,   IronCh↝, 1,  

Mitochondria & Bioenergetics(tgid=3)

ATP↑, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

adiP↓, 1,   ALAT↓, 1,   GlucoseCon↑, 1,   LDL↓, 1,  

Cell Death(tgid=5)

Akt↓, 1,   Apoptosis↓, 1,   iNOS↓, 1,   JNK↓, 1,   p‑JNK↓, 1,   MAPK↓, 1,   p38↓, 1,  

Transcription & Epigenetics(tgid=7)

Ach↑, 1,   other↑, 1,   other↝, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

GSK‐3β↓, 1,   HDAC↓, 1,   IGF-1↑, 1,  

Migration(tgid=13)

TGF-β1↑, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature(tgid=14)

NO↓, 4,  

Barriers & Transport(tgid=15)

BBB↑, 3,   GastroP↑, 1,   GLUT3↑, 1,   GLUT4↑, 1,  

Immune & Inflammatory Signaling(tgid=16)

COX2/PTGS2↓, 2,   CRP↓, 1,   IFN-γ↓, 1,   IL10↑, 1,   IL17↓, 1,   IL1β↓, 5,   IL6↓, 2,   Imm↑, 2,   Inflam↓, 8,   NF-kB↓, 3,   NK cell↑, 1,   TNF-α↓, 4,  

Synaptic & Neurotransmission(tgid=18)

5HT↑, 2,   AChE↓, 2,   ChAT↑, 2,   tau↓, 1,  

Protein Aggregation(tgid=19)

Aβ↓, 1,   XO↝, 1,  

Hormonal & Nuclear Receptors(tgid=20)

GR↑, 2,  

Drug Metabolism & Resistance(tgid=21)

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 2,   Dose↝, 1,   eff↓, 3,   eff↑, 1,   eff↝, 1,   Half-Life↓, 1,   Half-Life↑, 3,   Half-Life↝, 1,   P450↑, 1,  

Clinical Biomarkers(tgid=22)

ALAT↓, 1,   AST↓, 1,   BG↓, 1,   CRP↓, 1,   GutMicro↑, 2,   IL6↓, 2,  

Functional Outcomes(tgid=23)

AntiAge↑, 3,   AntiCan↑, 1,   AntiDiabetic↑, 1,   BOLD↑, 1,   cardioP↑, 5,   cognitive↑, 6,   hepatoP↑, 2,   memory↑, 9,   motorD↓, 1,   motorD↑, 1,   neuroP↑, 11,   Risk↓, 3,   Strength↑, 1,   toxicity↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24)

Diar↓, 1,  
Total Targets: 105

Scientific Paper Hit Count for: VitC, Vitamin C levels
4 Alpha-Lipoic-Acid
2 Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry
1 Anthocyanins
1 Ashwagandha(Withaferin A)
1 Chrysin
1 Chyawanprash
1 Shilajit/Fulvic Acid
1 HydroxyTyrosol
1 isoquercitrin
1 Lycopene
1 Rosmarinic acid
1 Selenium
1 chitosan
1 polyethylene glycol
1 Silymarin (Milk Thistle) silibinin
1 Thymoquinone
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#:%  Target#:1253  State#:%  Dir#:2
wNotes=on sortOrder:rid,rpid

 

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