Bax:Bcl2 Cancer Research Results
Bax:Bcl2, Bax:Bcl2 ratio: Click to Expand ⟱
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Bax and Bcl-2 are the major members of Bcl-2 family that play a key role in tumor progression or inhibition of intrinsic apoptotic pathway triggered by mitochondrial dysfunction.
Bax/Bcl-2 ratio is typically significantly lower in tumors.
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Scientific Papers found: Click to Expand⟱
*DNAdam↓, Our results showed that baicalein effectively inhibited H2O2-induced cytotoxicity and DNA damage associated with the inhibition of reactive oxygen species (ROS) accumulation.
*ROS↓,
*Bax:Bcl2↓, increased the Bax/Bcl-2 ratio
*p‑NRF2↑, baicalein increased not only the expression but also the phosphorylation of nuclear factor-erythroid 2 related factor 2 (Nrf2) and promoted the expression of heme oxygenase-1 (HO-1)
*HO-1↑, it is well known that the antioxidant efficacy of baicalein is related to the activation of the Nrf2/HO-1 signaling pathway
*neuroP↑, suggested that baicalein may have a beneficial effect on the prevention and treatment of peripheral neuropathy induced by oxidative stress.
*MMP↑, inhibitory effect of baicalein on MMP reduction
*ZO-1↓, Mechanisms showed that borneol as a “courier” opened up intercellular space and loosened the tight junctions of the nasal mucosa by suppressing ZO-1 and occludin expression
*cl‑Casp3↓, Osthole assisted by borneol demonstrated significantly improved efficiency in suppressing cleaved caspase-3 expression, increasing the Bcl-2/Bax ratio
*Bax:Bcl2↓,
*MDA↓, reducing malondialdehyde levels, inhibiting neuron apoptosis, and decreasing Aβ levels by inhibiting BACE1 expression to alleviate cognitive impairment in APP/PS1 mice
*Apoptosis↓,
*Aβ↓,
*BACE/β-secretase↓,
*cognitive↑,
*BioAv↑, our study demonstrated that the intracerebral bioavailability of osthole profoundly improved with intranasal administration of osthole/borneol
memory↑, our study demonstrated that the intracerebral bioavailability of osthole profoundly improved with intranasal administration of osthole/borneol
P-gp/ABCB1↓, This may be caused by a higher dose of BO inhibiting the action of the P-gp transporter in intestinal mucosa and CYP450 metabolism in the liver.
BioEnh↑,
*MDA↓, CAPE-loaded-NL significantly counteracted ornithine-induced elevation in serum activities of pancreatic digestive enzymes and pancreatic levels of malondialdehyde, nuclear factor kappa B (NF-κB) p65, tumor necrosis factor-alpha, nitrite/nitrate, clea
*NF-kB↓,
*p65↓,
*TNF-α↓,
*cl‑Casp3↓,
*GSR↑, pretreatment with CAPE-loaded-NL significantly reinstated the ornithine-lowered glutathione reductase activity, glutathione,
*GSH↑,
*NRF2↑, nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 levels and ATP/ADP ratio, and potentiated the Bcl-2/Bax ratio in pancreatic tissue.
*HO-1↑,
*Bax:Bcl2↓,
*antiOx↑, displayed superior antioxidant, anti-inflammatory and anti-apoptotic effects compared to free CAPE oral suspension
*Inflam↓,
*MMP↑, a reduction in mitochondrial membrane potential, an increased BAX/Bcl-2 ratio and consequently increased Poly (ADP-ribose) polymerase (PARP) cleavage. All these effects were blocked by EGb 761 treatment.
*Bax:Bcl2↓,
*cl‑PARP↓,
*i-antiOx↑, EGb 761, acting as intracellular antioxidant, protects neuroblastoma cells against activation of p53 mediated pathway and intrinsic mitochondrial apoptosis.
*mt-Apoptosis↓,
*neuroP↑, Our results suggest that EGb 761, protecting against oxidative-stress induced apoptotic cell death, could potentially be used as nutraceutical for the prevention and treatment of neurodegenerative diseases.
*Half-Life↓, Except the thigh muscle required a longer time to saturate, the other organs need 5–10 min to reach Cmax (maximum hydrogen concentration).
*ROS↓, regulate several key players in cancer, including ROS, and certain antioxidant enzymes
*selectivity↑, hydrogen gas could selectively scavenge the most cytotoxic ROS, •OH, as tested in an acute rat model of cerebral ischemia and reperfusion
*SOD↑, the expression of superoxide dismutase (SOD) (48), heme oxyganase-1 (HO-1) (49), as well as nuclear factor erythroid 2-related factor 2 (Nrf2) (50), increased significantly, strengthening its potential in eliminating ROS.
*HO-1↑,
*NRF2↑,
*chemoP↑, reduce the adverse effects in cancer treatment while at the same time doesn't abrogate the cytotoxicity of other therapy, such as radiotherapy and chemotherapy
*radioP↑,
ROS↑, Interestingly, due the over-produced ROS in cancer cells (38), the administration of hydrogen gas may lower the ROS level at the beginning, but it provokes much more ROS production as a result of compensation effect, leading to the killing of cancer
*Inflam↓, By regulating inflammation, hydrogen gas can prevent tumor formation, progression, as well as reduce the side effects caused by chemotherapy/radiotherapy
eff↑, More importantly, hydrogen-rich water didn't impair the overall anti-tumor effects of gefitinib both in vitro and in vivo, while in contrast, it antagonized the weight loss induced by gefitinib and naphthalene, and enhanced the overall survival rate
*TNF-α↓, hydrogen-rich saline treatment exerted its protective effects via inhibiting the inflammatory TNF-α/IL-6 pathway, increasing the cleaved C8 expression and Bcl-2/Bax ratio, and attenuating cell apoptosis in both heart and liver tissue
*IL6↓,
*cl‑Casp8↑,
*Bax:Bcl2↓,
*Apoptosis↓,
*cardioP↑,
*hepatoP↑,
*RenoP↑, Hydrogen-rich water also showed renal protective effect against cisplatin-induced nephrotoxicity in rats.
*chemoP↑, nother study showed that both inhaling hydrogen gas (1% hydrogen in air) and drinking hydrogen-rich water (0.8 mM hydrogen in water) could reverse the mortality, and body-weight loss caused by cisplatin via its anti-oxidant property
eff↝, More importantly, hydrogen didn't impair the anti-tumor activity of cisplatin against cancer cell lines in vitro and in tumor-bearing mice
chemoP↑, hydrogen-rich water combinational treatment group exhibited no differences in liver function during the treatment, probably due to its antioxidant activity, indicating it a promising protective agent to alleviate the mFOLFOX6-related liver injury
radioP↑, consumption of hydrogen-rich water reduced the radiation-induced oxidative stress while at the same time didn't compromise anti-tumor effect of radiotherapy
eff↑, Hydrogen Gas Acts Synergistically With Thermal Therapy
TumCG↓, in vivo study showed that under hydrogen gas treatment, tumor growth was significantly inhibited, as well as the expression of Ki-67, VEGF and SMC3
Ki-67↓,
VEGF↓,
selectivity↑, H2-silica could concentration-dependently inhibit the cell viability of human esophageal squamous cell carcinoma (KYSE-70) cells, while it need higher dose to suppress normal human esophageal epithelial cells (HEEpiCs), indicating its selective profi
*ROS↓, HuA improves synaptic plasticity and decreases ROS level in CIH mice
*cognitive↑, HuA significantly improved cognitive impairment and neuronal damage in the hippocampus of CIH mice via increasing the ratio of Bcl-2/Bax and inhibiting caspase-3 cleavage.
*neuroP↑,
*Bax:Bcl2↓,
*Casp3↑,
*NADPH↓, HuA considerably decreased ROS levels by downregulating the high levels of NADPH oxidase (NOX 2, NOX 4) mediated by CIH.
*NOX↓,
*TfR1/CD71↓, Decreased levels of TfR1 and FTL proteins observed in HuA treated CIH group, could reduce iron overload in hippocampus. HuA increased PSD 95 protein expression, CREB activation and BDNF protein expression
*Iron↓,
*PSD95↑,
*BDNF↑,
selectivity↑, Here we show that CA1a cells are more sensitive to low concentration of I3C in terms of cell growth inhibition compared to MCF10A cells.
Bax:Bcl2↓, I3C upregulates Bax/Bcl-2 ratio and downregulates Bcl-xL expression in CA1a cells but not in MCF10A cells.
Bcl-xL↓,
BAX↑, that I3C induces Bax translocation to the mitochondria, causing mitochondrial depolarization, resulting in the loss of mitochondrial potential leading to the release of cytochrome c and subsequent cell death in CA1a cells but not in MCF10A cells.
MMP↓,
Cyt‑c↑,
TumCD↑,
*BioAv↓, Although ISLT has been globally recognized for its health benefits, its oral administration is still restricted by sparing water solubility, poor bioavailability, and slow dissolution in the intestine.
GlucoseCon↓, ISLT (MGC803 cells: 40 μM, SGC7901 cells: 50 µM) downregulated the expression of glucose transporter four and reduced the uptake of glucose by GC cells.
LDH↓, demonstrated that it suppressed the activity of lactate dehydrogenase and pyruvate dehydrogenase kinase 1 and reduced the production of glycolytic products.
PDK1↓,
Glycolysis↓,
mt-OXPHOS↓, It impaired mitochondrial function while simultaneously suppressing glycolysis and inhibiting mitochondrial oxidative phosphorylation, ultimately leading to energy metabolic collapse in GC cells.
Bax:Bcl2↓, it decreased the Bcl-2/Bax ratio and upregulated cleaved caspase-3/caspase-9 to promote GC cell apoptosis.
cl‑Casp3↑,
cl‑Casp9↑,
Apoptosis↑,
Hif1a↓, hypoxia-inducible factor-1α was downregulated to regulate the energy metabolism and proliferative activity of GC cells
ROS↑, ISLT-17 increases the production of Reactive oxygen species (ROS) in GC cells, thereby inhibiting cell growth.
*AntiDiabetic↑, ISLT possesses therapeutic effects on various diseases such as diabetes, cardiovascular diseases, and kidney diseases by activating the Nrf2 pathway
*cardioP↑,
*RenoP↑, structure in patients with diabetic kidney disease, inhibited oxidative stress and reduced ROS levels, and suppressed the activation of NF-kappa B and NLRP3 inflammasomes and the occurrence of pyroptosis, which played a renal protective role
*ROS↓,
*NF-kB↓,
*NLRP3↓,
*Pyro↓,
*antiPs↑, ISLT (1 mg/kg/day and 2 mg/kg/day) ameliorates psoriasis by inhibiting IL-6 and IL-8 and inhibiting inhibitory nuclear factor-kappa B activity, resulting in a reduction in pro-inflammatory.
*IL6↓,
*IL8↓,
BioAv↑, Compared with traditional oral and injectable methods, transdermal administration possesses significant advantages, such as protection against first-pass effects, improved bioavailability, enhanced patient compliance, prolonged drug stability, and th
BioAv↑, Accordingly, transdermal drug delivery systems containing intercellular lipid components (ceramides) can effectively improve the transdermal efficiency of lipophilic drugs, including ISLT.
BioAv↑, ISLT@NPs possessed significantly higher targeted accumulation in the colon and improved tissue penetration than free DiR, suggesting higher oral bioavailability.
*Learn↑, ISL pretreatment reversed these deficits as well as LPS-induced decreases in the hippocampal expression levels of synaptophysin, postsynaptic density-95, brain-derived neurotrophic factor, superoxide dismutase, glutathione peroxidase, and BCL-2.
*PSD95↑,
*BDNF↑,
*SOD↑,
*GPx↑,
*Bcl-2↑,
*SYP↑,
*Bax:Bcl2↓, ISL pretreatment also reversed LPS-induced increases in TUNEL-positive (apoptotic) cells, BAX/BCL-2 ratio, and expression levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and C-C motif chemokine ligand 3.
*TNF-α↓,
*IL1β↓,
*IL6↓,
*MIP‑1α/CCL3↓,
*p‑GSK‐3β↑, Pretreatment with ISL increased the expression levels of phosphorylated (p)-GSK-3β, nuclear NRF2, HO-1 mRNA, and NQO1 mRNA, and reversed LPS-induced nuclear translocation of nuclear factor (NF)-κB
*NRF2↑,
*HO-1↑,
*NQO1↑,
*cognitive↑, ISL protects against LPS-induced cognitive impairment and neuronal injury by promoting or maintaining antioxidant capacity and suppressing neuroinflammation, likely through phosphorylation-dependent inactivation of GSK-3β, enhanced expression of NRF
*Inflam↓,
*hepatoP↑, ISL significantly improved the liver pathological changes.
*ROS↓, ISL reduced oxidative stress by altering the expression of PGC-1α, Nrf2, HO-1, NQO1, Keap1, GCLC, and GCLM in damaged hepatocytes.
*PGC-1α↝,
*NRF2↑,
*HO-1↑,
*NQO1↝,
*Keap1↝,
*GCLC↝,
*GCLM↝,
*NLRP3↓, NLRP3 inflammasome, IL-1β, IL-6, TNF-α, iNOS, and Mip-2 were repressed by ISL.
*IL1β↓,
*IL6↓,
*TNF-α↓,
*MIP2↓,
*Bax:Bcl2↓, ISL alleviated LPS/D-GalN-induced hepatocytes apoptosis by increasing the Bcl-2/Bax ratio and suppressing the expression of cleaved caspase-3.
*cl‑Casp3↓,
*Inflam↓, ISL improves the ability of anti-oxidative stress, alleviates inflammatory reaction, apoptosis, and inhibits NLRP3 inflammasome
*Apoptosis↓,
*cognitive↑, ISO improved systemic glucose metabolism and alleviated hepatic steatosis, and reversed cognitive deficits.
*PSD95↑, ISO restored synaptic proteins (PSD-95, BDNF, soluble α-synuclein), exerted anti-apoptotic effects (increased Bcl-2/Bax ratio, decreased cleaved caspase-3), and attenuated oxidative stress and mitochondrial damage.
*BDNF↑,
*Bax:Bcl2↓,
*cl‑Casp3↓,
*ROS↓,
*mtDam↓,
*GSK‐3β↓, Mechanistically, ISO inhibited GSK3β activity, promoted Nrf2 nuclear accumulation, upregulated HO-1 expression, and reduced tau phosphorylation at Ser396
*NRF2↑,
*HO-1↑,
*p‑tau↓,
*neuroP↑, ISO exerts a neuroprotective effect in TDACD model by inhibiting oxidative stress via GSK3β/Nrf2 pathway, and highlight ISO as a potential therapeutic candidate for TDACD.
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*Inflam↓, luteolin, showing significant anti-inflammatory, antioxidant, and neuroprotective activity.
*antiOx↑,
*neuroP↑,
*BioAv↝, To increase the bioavailability of luteolin, several delivery methods have been developed; the most thoroughly studied include lipid carriers like liposomes and nanoformulations
*BBB↑, luteolin given intraperitoneally (ip) to mice can readily cross the blood-brain barrier (BBB) and enter the brain
*TNF-α↓, nhibiting pro-inflammatory mediators such as cyclooxygenase-2 (COX-2), nitric oxide (NO), TNF-α, IL-β, IL-6, IL-8, IL-31, and IL-33 in several in vitro models of AD
*IL1β↓,
*IL6↓,
*IL8↓,
*IL33↓,
*NF-kB↓, inhibition of the NF-кB pathway
*BACE/β-secretase↓, leads to the inhibition of a downstream target– β-site amyloid precursor protein cleaving enzyme (BACE1), which is a key mediator in forming Aβ fibrils in AD pathology
*ROS↓, anti-oxidant activity mainly by reducing ROS levels and increasing SOD activity in in vitro models of AD
*SOD↑,
*HO-1↑, increase the expression of antioxidant enzymes such as heme oxygenase-1 (HO-1) via the nuclear factor erythroid 2–related factor 2/ antioxidant responsive element (Nrf-2/ARE) complex activation
*NRF2↑,
*Casp3↓, reducing the levels of caspase-3 and − 9 and improving the B-cell lymphoma protein 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, as it was reported in in vitro models of AD
*Casp9↑,
*Bax:Bcl2↓,
*UPR↑, enhancing the unfolded protein response (UPR) pathway, leading to an increase in endoplasmic reticulum (ER) chaperone GRP78 and a decrease in the expression of UPR-targeted pro-apoptotic genes via the MAPK pathway.
*GRP78/BiP↑,
*Aβ↓, evidence that suggests that luteolin can directly influence the formation of Aβ plaques by selectively inhibiting the activity of N-acetyl-α-galactosaminyltransferase (ppGalNAc-T) isoforms
*GSK‐3β↓, inactivating the glycogen synthase kinase-3 alpha (GSK-3α) isoform, suppressing Aβ and promoting tau disaggregation
*tau↓,
*CREB↑, luteolin promoted phosphorylation and activation of cAMP response element-binding protein (CREB) leading to the increased miR-132 expression, and eventually neurite outgrowth in PC12 cells
*ATP↑, ROS production was decreased by 40%, MMP levels were restored close to control N2a levels (202%), and ATP levels were improved by 444%).
*cognitive↑, protective effect of luteolin against cognitive dysfunction was also reported in the streptozotocin
*BloodF↑, Luteolin increased regional cerebral blood flow values, alleviated the leakage of the lumen of vessels, and protected the integrity of BBB
*BDNF↑, increasing the level of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor (TrkB) expression in the cerebral cortex
*TrkB↑,
*memory↑, luteolin supplementation significantly ameliorated memory and cognitive deficits in 3 × Tg-AD mice.
*PPARγ↑, attenuated mitochondrial dysfunction via peroxisome proliferator-activated receptor gamma (PPARγ) activation.
*eff↑, combination of luteolin with another compound– l-theanine (an amino acid found in tea) also improved AD-like symptoms in the Aβ25–35-treated rats
*motorD↑, naringin-treated animals had significantly better locomotor function recovery, less myelin loss, and higher expression of BDNF and VEGF.
*BDNF↑,
*VEGF↑,
*Bax:Bcl2↓, naringin treatment significantly increased in Bcl-2:Bax ratio, reduced the enzyme activity of caspase-3 and decreased the number of apoptotic cells after SCI.
*Casp3↓,
*Apoptosis↓,
*eff↑, findings suggest that naringin treatment starting 1 day after SCI can significantly improve locomotor recovery, and this neuroprotective effect may be related to the upregulation of BDNF and VEGF and the inhibition of neural apoptosis.
*Bcl-2↑,
*BAX↓,
*Bax:Bcl2↓, Que postconditioning significantly decreased Bax expression and increased Bcl-2 expression
*cardioP↑, cardioprotection by activating the PI3K/Akt signaling pathway and modulating the expression of Bcl-2 and Bax proteins.
*Akt↑,
*PI3K↑,
*LDH↓, Que postconditioning reduced the levels of CK (1642.9±194.3 vs 2679.5±194.3 U/L, P<0.05) and LDH (1273.6±176.5 vs 2618±197.7 U/L, P<0.05) compared to the I/R group
*ALAT↓, N. sativa oil (0.1 and 0.2 mL/kg) diminished the levels of the biochemical markers ALT and AST.
*AST↓,
*lipid-P↓, Administration of black seed oil (0.1, 0.2 and 0.5 mL/kg) reduced lipid peroxidation
*GSH↑, and at doses 0.1 and 0.2 mL/kg significantly recovered the GSH content.
*Bax:Bcl2↓, The oil decreased Bax/Bcl2 levels and at 0.1 mL/kg down-regulated the expressions of caspase-3
*proCasp3↓,
*cl‑Casp3↓,
*antiOx↑, Through its antioxidant and anti-apoptosis properties, black seed oil exhibited an anti-aging effect in a model of aging induced with D-galactose.
Showing Research Papers: 1 to 15 of 15
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
mt-OXPHOS↓, 1, ROS↑, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
GlucoseCon↓, 1, Glycolysis↓, 1, LDH↓, 1, PDK1↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 1, BAX↑, 1, Bax:Bcl2↓, 2, Bcl-xL↓, 1, cl‑Casp3↑, 1, cl‑Casp9↑, 1, Cyt‑c↑, 1, TumCD↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
TumCG↓, 1,
Migration(tgid=13) ⓘ
Ki-67↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
Hif1a↓, 1, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 3, BioEnh↑, 1, eff↑, 2, eff↝, 1, selectivity↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
Ki-67↓, 1, LDH↓, 1,
Functional Outcomes(tgid=23) ⓘ
chemoP↑, 1, memory↑, 1, radioP↑, 1,
Total Targets: 30
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
Learn↑, 1, SYP↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 3, i-antiOx↑, 1, GCLC↝, 1, GCLM↝, 1, GPx↑, 1, GSH↑, 2, GSR↑, 1, HO-1↑, 7, Iron↓, 1, Keap1↝, 1, lipid-P↓, 1, MDA↓, 2, NQO1↑, 1, NQO1↝, 1, NRF2↑, 6, p‑NRF2↑, 1, ROS↓, 7, SOD↑, 3,
Metal & Cofactor Biology(tgid=2) ⓘ
TfR1/CD71↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, MMP↑, 2, mtDam↓, 1, PGC-1α↝, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, CREB↑, 1, LDH↓, 1, NADPH↓, 1, PPARγ↑, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 1, Apoptosis↓, 4, mt-Apoptosis↓, 1, BAX↓, 1, Bax:Bcl2↓, 13, Bcl-2↑, 2, Casp3↓, 2, Casp3↑, 1, cl‑Casp3↓, 5, proCasp3↓, 1, cl‑Casp8↑, 1, Casp9↑, 1, Pyro↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
GRP78/BiP↑, 1, UPR↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, cl‑PARP↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↓, 2, p‑GSK‐3β↑, 1, PI3K↑, 1,
Migration(tgid=13) ⓘ
ZO-1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
VEGF↑, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
IL1β↓, 3, IL33↓, 1, IL6↓, 5, IL8↓, 2, Inflam↓, 5, MIP‑1α/CCL3↓, 1, MIP2↓, 1, NF-kB↓, 3, p65↓, 1, TNF-α↓, 5,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
BDNF↑, 5, PSD95↑, 3, tau↓, 1, p‑tau↓, 1, TrkB↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 2, BACE/β-secretase↓, 2, NLRP3↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 1, BioAv↝, 1, eff↑, 2, Half-Life↓, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, BloodF↑, 1, IL6↓, 5, LDH↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiDiabetic↑, 1, antiPs↑, 1, cardioP↑, 3, chemoP↑, 2, cognitive↑, 5, hepatoP↑, 2, memory↑, 1, motorD↑, 1, neuroP↑, 5, radioP↑, 1, RenoP↑, 2,
Total Targets: 94
Scientific Paper Hit Count for: Bax:Bcl2, Bax:Bcl2 ratio
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
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