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↓,
*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↓, 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↓,
*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↑,
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Park, |
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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↓, 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 9 of 9
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↑, 1,
Proliferation, Differentiation & Cell State ⓘ
TumCG↓, 1,
Migration ⓘ
Ki-67↓, 1,
Angiogenesis & Vasculature ⓘ
VEGF↓, 1,
Barriers & Transport ⓘ
P-gp↓, 1,
Drug Metabolism & Resistance ⓘ
BioEnh↑, 1, eff↑, 2, eff↝, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
Ki-67↓, 1,
Functional Outcomes ⓘ
chemoP↑, 1, memory↑, 1, radioP↑, 1,
Total Targets: 13
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, GSH↑, 2, GSR↑, 1, HO-1↑, 4, Iron↓, 1, lipid-P↓, 1, MDA↓, 2, NRF2↑, 3, p‑NRF2↑, 1, ROS↓, 4, SOD↑, 2,
Metal & Cofactor Biology ⓘ
TfR1/CD71↓, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, CREB↑, 1, LDH↓, 1, NADPH↓, 1, PPARγ↑, 1,
Cell Death ⓘ
Akt↑, 1, Apoptosis↓, 3, BAX↓, 1, Bax:Bcl2↓, 9, Bcl-2↑, 1, Casp3↓, 2, Casp3↑, 1, cl‑Casp3↓, 3, proCasp3↓, 1, cl‑Casp8↑, 1, Casp9↑, 1,
Protein Folding & ER Stress ⓘ
GRP78/BiP↑, 1, UPR↑, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State ⓘ
GSK‐3β↓, 1, PI3K↑, 1,
Migration ⓘ
ZO-1↓, 1,
Angiogenesis & Vasculature ⓘ
VEGF↑, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
IL1β↓, 1, IL33↓, 1, IL6↓, 2, IL8↓, 1, Inflam↓, 3, NF-kB↓, 2, p65↓, 1, TNF-α↓, 3,
Cellular Microenvironment ⓘ
NOX↓, 1,
Synaptic & Neurotransmission ⓘ
BDNF↑, 3, PSD95↑, 1, tau↓, 1, TrkB↑, 1,
Protein Aggregation ⓘ
Aβ↓, 2, BACE↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, BioAv↝, 1, eff↑, 2, Half-Life↓, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, BloodF↑, 1, IL6↓, 2, LDH↓, 1,
Functional Outcomes ⓘ
cardioP↑, 2, chemoP↑, 2, cognitive↑, 3, hepatoP↑, 1, memory↑, 1, motorD↑, 1, neuroP↑, 3, radioP↑, 1, RenoP↑, 1,
Total Targets: 72
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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