TBARS Cancer Research Results
TBARS, Thiobarbituric Acid Reactive Substances: Click to Expand ⟱
| Source: |
| Type: measure |
TBARS (Thiobarbituric Acid Reactive Substances) is a measure of lipid peroxidation, which is the oxidative degradation of lipids. Lipid peroxidation is a process in which free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs), leading to cell damage.
Research has shown that TBARS levels are often elevated in cancer patients. This is because cancer cells have higher levels of reactive oxygen species (ROS) than normal cells, which can lead to increased lipid peroxidation.
|
Scientific Papers found: Click to Expand⟱
| - |
Review, |
CardioV, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*Inflam↓, allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others).
*antiOx↑, improving the antioxidant system
*neuroP↑,
*cardioP↑,
*AntiTum↑,
*mtDam↑, Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes.
*HSP70/HSPA5↑, llicin improves mitochondrial function by enhancing the expression of HSP70 and decreasing RAAS activation
*NRF2↑,
*RAAS↓,
*cognitive↑, Allicin enhances the cognitive function of APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice by decreasing the expression levels of Aβ, oxidative stress, and improving mitochondrial function.
*SOD↑, positive effects on cognition in an AD mouse model by administrating a preventive dose of allicin. These effects might be mediated by an increase of SOD and reduction of ROS
*ROS↓,
*NRF2↑, Chronic treatment with allicin increased the expression of NRF2 and targeted downstream of NRF2, such as NADPH, quinone oxidoreductase 1 (NQO1), and γ-glutamyl cysteine synthetase (γ-GCS), in the hippocampus of aged mice
*ER Stress↓, protective effects of 16 weeks of allicin treatment in a rat model of endoplasmic reticulum stress-related cognitive deficits.
*neuroP↑, allicin was able to ameliorate depressive-like behaviors by decreasing neuroinflammation, oxidative stress iron
aberrant accumulation,
*memory↑, allicin improved lead acetate-caused learning and memory deficits and decreased the ROS level
*TBARS↓, Oral administration of allicin was able to reduce thiobarbituric reactive substances (TBARS) and
myeloperoxidase (MPO) levels, and concurrently increased (SOD) activity, glutathione S-transferase (GST) and glutathione (GSH) levels in a rat model of
*MPO↓,
*SOD↑,
*GSH↑,
*iNOS↓, decreasing the expression of iNOS and increased the phosphorylation of endothelial NOS (eNOS)
*p‑eNOS↑,
*HO-1↑, OSCs upregulate the endogenous antioxidant NRF2 and heme oxygenase-1 (HO-1)
| - |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
Park, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
Park, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,
| - |
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↓,
*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
Bcl-2↓, Crocin significantly reduced cell viability of BXPC3 and Capan-2 by triggering caspase signaling via the downregulation of Bcl-2.
Apoptosis↑, crocin treatment-induced apoptosis by inducing the release of cytochrome c from mitochondria to cytosol.
Cyt‑c↑,
TumCG↓, In mice bearing pancreatic tumors, crocin significantly reduced tumor burden without a change in body weight.
radioP↑, Additionally, it showed significant protection against radiation-induced hepatic oxidative damage, reduced the levels of hepatic toxicity and preserved liver morphology.
TumCCA↑, Various studies have shown that carotenoids of saffron extract, crocin and crocetin, arrest the cell cycle at S, G0/G1and G2/M stages [26,27,28,29,30,31,32,33,34], inhibiting mitosis, cell proliferation and triggering apoptosis.
TumCP↓,
DNAdam↑, crocin induces DNA fragmentation, apoptosis and cell cycle arrest at the G1 phase in Bx-PC-3 pancreatic cancer cells
TBARS↓, Crocin showed dose-dependent inhibition of TBARS
P53↑, Crocin upregulated P53, P38, cytochrome c, P21cip1 and P27kip1, whereas CDK2 and c-Myc were downregulated dose-dependently in BXPC3 and Capan-2 cells
p38↑,
CDK2↓,
cMyc↓,
*MDA↓, IR (4Gy) increased the MDA levels in mice and crocin treatment restores the MDA level
GSH↑, In this study, increased GSH level (Table 1) suggests that protection by the crocin mediated through the restoration of IR altered hepatic antioxidant status (Table 1 and Table 2).
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*Inflam↓, wide spectrum of pharmacological activities including anti-inflammatory, anticancer, antimicrobial, antioxidant, and neuroprotective activities.
*AntiCan↑,
*AntiBio↑,
*antiOx↑,
*neuroP↑,
ROS↓, GNL scavenges free radicals and preserves the activity of antioxidant enzymes.
Apoptosis↑, GNL induces apoptosis and cell cycle arrest, modulates multiple molecular targets, including p53 and STAT3, activates caspases, and modulates inflammation via transcriptional regulation.
TumCCA↑,
P53↝,
STAT3↓, GNL reduces survivin protein levels by downregulating phosphorylated STAT3.
Casp↝,
*Catalase↑, This compound protects various antioxidant enzymes, such as catalase, glutathione-S-transferase, and glutathione peroxidase.
*GSTs↑,
*GPx↑,
*AChE↓, In addition, GNL suppressed acetylcholinesterase (AChE) activity and alleviated oxidative stress by boosting neuronal reduced glutathione (GSH), catalase (CAT), glutathione-S-transferase (GST), and superoxide dismutase (SOD) activities.
*GSH↑,
*SOD↑,
*TBARS↓, It lowered malondialdehyde concentration (TBARS), nitric oxide (NO), and xanthine oxidase (XO), and restored the structural damage to the brain tissue caused by HFD.
*NO↓,
*XO↓,
*memory↑, GNL boosted learning and memory function and ameliorated the inflammation status in the brain by lowering the protein levels of IL-1β, iNOS, NF-κBp65, and COX-2
*IL1β↓,
*iNOS↓,
*NF-kB↓,
*COX2↓,
*NRF2↑, GNL administration ameliorated renal function, alleviated histological changes, and enhanced Nrf-2/HO-1/NQO-1 with a subsequent intensification of antioxidant enzyme activities.
*HO-1↑,
*survivin↓, GNL reduces survivin protein levels by downregulating phosphorylated STAT3.
TumCP↓, They have shown that GNL treatment significantly suppressed oral squamous cell carcinoma (OSCC) cell proliferation and migration in vitro and tumor growth in vivo in a time- and dose-dependent manner.
TumCMig↓,
TumCG↑,
selectivity↑, GNL may be helpful in treating different types of malignancy, while having limited effects on normal cells.
TumMeta↓, GNL has been reported to inhibit cancer metastasis and angiogenesis.
angioG↓,
Hif1a↓, A549 lung cancer cells treated with GNL, downregulation of HIF-1alpha, a VEGF regulator, occurred
Beclin-1↓, GNL also decreases autophagy through downregulation of BNIP3 and beclin-1 expression, which increases apoptotic cell death through HIF-1α signaling.
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) ⓘ
GSH↓, 1, GSH↑, 1, ROS↓, 1, ROS↑, 1, TBARS↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
cMyc↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↑, 3, Bak↓, 1, BAX↑, 1, Bcl-2↓, 3, BID↑, 1, Casp↝, 1, Casp12↑, 1, Casp3↑, 2, Casp8↑, 2, Casp9↑, 2, Cyt‑c↑, 3, Fas↑, 2, p38↑, 2,
Kinase & Signal Transduction(tgid=6) ⓘ
HER2/EBBR2↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
CHK1↓, 1, DNAdam↑, 1, P53↑, 3, P53↝, 1, PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK2↓, 1, CycB/CCNB1↓, 1, P21↑, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
FGF↓, 1, STAT3↓, 2, TumCG↓, 1, TumCG↑, 1,
Migration(tgid=13) ⓘ
CEA↓, 1, p‑FAK↓, 1, TIMP2↑, 1, TumCMig↓, 2, TumCP↓, 2, TumMeta↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, EGFR↑, 1, Hif1a↓, 2, VEGF↓, 1, VEGFR2↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 1, IL8↓, 1, NF-kB↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
CEA↓, 1, EGFR↑, 1, HER2/EBBR2↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, chemoP↑, 1, radioP↑, 1,
Total Targets: 58
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiBio↑, 3,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 5, Catalase↑, 4, GPx↑, 2, GSH↑, 6, GSTs↑, 2, HO-1↑, 3, Keap1↓, 1, Keap1↑, 1, lipid-P↓, 3, MDA↓, 4, MPO↓, 2, NRF2↑, 5, ROS↓, 6, SOD↑, 7, TBARS↓, 5, uricA↓, 1, VitC↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, MMP↑, 1, mtDam↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, H2S↑, 1, LDH↓, 2,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↓, 2, BAX↓, 1, Bcl-2↑, 1, Casp3↓, 1, Cyt‑c↓, 1, iNOS↓, 6, JNK↓, 1, survivin↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↓, 1, HSP70/HSPA5↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↓, 1, HDAC↓, 1, PI3K↓, 1,
Migration(tgid=13) ⓘ
MMP13↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
p‑eNOS↑, 1, NO↓, 3,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 2, GastroP↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 1, COX2↓, 5, IFN-γ↓, 1, IL17↓, 1, IL1β↓, 3, IL6↓, 2, IL6↑, 1, Imm↑, 1, Inflam↓, 5, NF-kB↓, 3, PGE2↓, 1, TNF-α↓, 4,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 3, BChE↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE↓, 1, XO↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
GR↑, 1, RAAS↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 2, eff↑, 2, Half-Life↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, BP↓, 1, creat↓, 2, GutMicro↑, 1, IL6↓, 2, IL6↑, 1, LDH↓, 2,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, AntiTum↑, 1, cardioP↑, 4, cognitive↑, 2, hepatoP↑, 1, memory↑, 4, motorD↑, 1, neuroP↑, 7, Pain↓, 1, RenoP↑, 1, toxicity↓, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, CD8+↑, 1,
Total Targets: 87
Scientific Paper Hit Count for: TBARS, Thiobarbituric Acid Reactive Substances
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#:862 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
Home Page