PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25892964-7 2015 Second, insulin pre-administration could significantly reduce apoptosis and ameliorate mitochondrial dysfunction in liver of mice exposed to ethanol, supporting by decreasing caspases-3 activities and the ratio of Bax/Bcl-2, increasing mitochondrial viability and mitochondrial oxygen consumption, inhibition of the decline of ATP levels and mitochondrial ROS accumulation. Ethanol 141-148 BCL2-associated X protein Mus musculus 214-217 20090911-8 2010 Myocardium from ethanol-treated mice displayed enhanced Bax, Caspase-3 and decreased Bcl-2 expression, the effect of which with the exception of Caspase-3 was augmented by ADH. Ethanol 16-23 BCL2-associated X protein Mus musculus 56-59 25084483-10 2014 Rutin significantly reversed ethanol-increased Bax, cytochrome c expression and caspase 3 activity, and decreased Bcl-2 and Bcl-xL protein expression in HT22 cells. Ethanol 29-36 BCL2-associated X protein Mus musculus 47-50 22982332-8 2012 Compounds also inhibited the cleavage of PARP and bax and restored Bcl2, induced on exposure to ethanol. Ethanol 96-103 BCL2-associated X protein Mus musculus 50-53 21434306-0 2011 [Effect of grape procyanidins on expressions of Caspase-3 and Bax in ethanol-induced liver injury in mice]. Ethanol 69-76 BCL2-associated X protein Mus musculus 62-65 20803734-7 2010 The present study has indicated that the ethanol treatment induced apoptosis in the mouse testis through the increased expression of Fas/Fas-L and p53, up-regulation of Bax/Bcl-2 ratio, cytosolic translocation of cytochrome c along with caspase-3 activation and glutathione depletion. Ethanol 41-48 BCL2-associated X protein Mus musculus 169-172 22211272-8 2012 Furthermore, ethanol induced significantly higher ROS generation in EL-4 cells as compared to lymphocytes and caused PARP cleavage and activation of apoptotic proteins like p53 and Bax, in EL-4 cells and not in normal lymphocytes. Ethanol 13-20 BCL2-associated X protein Mus musculus 181-184 22211272-10 2012 Taken together, these results suggest that ethanol upto a concentration of 5% caused no significant immunotoxicity towards normal lymphocytes and induced cell death in EL-4 cells via phosphorylation of p38MAPK and regulation of p53 leading to further activation of both extrinsic (Fas) and intrinsic (Bax) apoptotic markers. Ethanol 43-50 BCL2-associated X protein Mus musculus 301-304 21434306-7 2011 CONCLUSION: GPC could suppressing the expression of Caspase-3 and Bax in the liver of mice with ethanol-induced liver injury. Ethanol 96-103 BCL2-associated X protein Mus musculus 66-69 20803734-5 2010 Western blot analysis revealed that repeated ethanol treatment decreased the expression of steroidogenic acute regulatory protein (StAR), 3 beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17beta-HSD); increased the expression of active caspase-3, p53, Fas and Fas-L; and led to up-regulation of Bax/Bcl-2 ratio and translocation of cytochrome c from mitochondria to cytosol in testis. Ethanol 45-52 BCL2-associated X protein Mus musculus 335-338 17448893-8 2007 The mitochondria from the ethanol-fed Sod1-/- mice had elevated levels of cleaved Bax, Bak, Bcl-xl, and adenine nucleotide translocator. Ethanol 26-33 BCL2-associated X protein Mus musculus 82-85 19382207-6 2009 Ethanol induced dephosphorylation of GSK3beta at Ser9 and the activation of Bax as well as caspase-3 in the developing mouse brain. Ethanol 0-7 BCL2-associated X protein Mus musculus 76-79 16738485-0 2006 Prion protein protects against ethanol-induced Bax-mediated cell death in vivo. Ethanol 31-38 BCL2-associated X protein Mus musculus 47-50 16738485-2 2006 To determine whether prion protein can protect against Bax-mediated cell death in vivo, wild-type, null and prion over-expressing mice were subjected to Bax-dependent ethanol induced neuronal apoptotic cell death and the brains were immunostained for active caspase-3 as a downstream marker of Bax activation. Ethanol 167-174 BCL2-associated X protein Mus musculus 153-156 16738485-2 2006 To determine whether prion protein can protect against Bax-mediated cell death in vivo, wild-type, null and prion over-expressing mice were subjected to Bax-dependent ethanol induced neuronal apoptotic cell death and the brains were immunostained for active caspase-3 as a downstream marker of Bax activation. Ethanol 167-174 BCL2-associated X protein Mus musculus 153-156 16738485-3 2006 Bax activation occurs in all ethanol-injected mice independent of their genotype. Ethanol 29-36 BCL2-associated X protein Mus musculus 0-3 14502238-0 2003 Ethanol-induced neuronal apoptosis in vivo requires BAX in the developing mouse brain. Ethanol 0-7 BCL2-associated X protein Mus musculus 52-55 16215995-5 2006 bax knock-out and wild-type mice pups were exposed to ethanol via vapor inhalation during the maximal period of neonatal cerebellar ethanol sensitivity and cerebellar tissue was subsequently assessed for Purkinje and granule cell number and ethanol-mediated generation of reactive oxygen species (ROS). Ethanol 54-61 BCL2-associated X protein Mus musculus 0-3 14502238-8 2003 Therefore, it appears that ethanol-induced neuroapoptosis is an intrinsic pathway-mediated phenomenon involving Bax-induced disruption of mitochondrial membranes and cytochrome c release as early events leading to caspase-3 activation. Ethanol 27-34 BCL2-associated X protein Mus musculus 112-115 12043192-0 2002 Changes of bcl-2 and bax mRNA expressions in the ethanol-treated mouse brain. Ethanol 49-56 BCL2-associated X protein Mus musculus 21-24 12163104-3 2002 In addition, it was shown that ethanol induces increases in levels of bax and caspase-3 and a decrease in bcl-2 expression. Ethanol 31-38 BCL2-associated X protein Mus musculus 70-73 12043192-1 2002 To characterize the biochemical mechanism of cell death induced by ethanol intoxication, we examined expression of mRNAs of bcl-2 and bax genes in the brain, which are related to apoptosis, by using the reverse transcription-polymerase chain reaction method (RT-PCR). Ethanol 67-74 BCL2-associated X protein Mus musculus 134-137 12043192-6 2002 We found that bcl-2 or bax mRNA expressions in the brain were changed after short-term ethanol exposure. Ethanol 87-94 BCL2-associated X protein Mus musculus 23-26 12043192-7 2002 These results suggest that bcl-2 or bax may have functional significance about ethanol intoxication. Ethanol 79-86 BCL2-associated X protein Mus musculus 36-39 29138110-2 2018 The present study tested the hypothesis that ethanol exposure during the period of naturally occurring neuronal death causes a time- and Bax-dependent neuronal loss. Ethanol 45-52 BCL2-associated X protein Mus musculus 137-140 33973356-13 2021 Ethanol promoted Bax expression and cytochrome C release and inhibited Bcl-2 and ATP expression. Ethanol 0-7 BCL2-associated X protein Mus musculus 17-20 35356144-8 2022 Treadmill exercise suppressed ethanol with LPS and CCl4-mediated elevation of Bax expression and increased Bcl-2 expression suppressed by application of ethanol with LPS and CCl4. Ethanol 30-37 BCL2-associated X protein Mus musculus 78-81 35356144-8 2022 Treadmill exercise suppressed ethanol with LPS and CCl4-mediated elevation of Bax expression and increased Bcl-2 expression suppressed by application of ethanol with LPS and CCl4. Ethanol 153-160 BCL2-associated X protein Mus musculus 78-81 33713693-11 2021 GluA1 silencing aggravated ethanol-induced changes in cell viability and apoptosis and the expression of BDNF, BAX and cleaved caspase-3, and GluA1 overexpression attenuated these changes. Ethanol 27-34 BCL2-associated X protein Mus musculus 111-114 33430871-10 2021 CONCLUSION: Lactate mitigates ethanol-induced GMI by curtailing local gastric inflammatory response, down-regulating the expression of the apoptosis regulator and executor genes Bax and Casp3, and up-regulating the expression of genes encoding tight junction proteins Occludin, Claudin-1, and Claudin-5 and the lactate receptor GPR81. Ethanol 30-37 BCL2-associated X protein Mus musculus 178-181 29431616-8 2018 Also, PXR-dependent was the binge EtOH-induced inhibition of hepatic Akr1b8 mRNA, and protein levels of aldehyde dehydrogenase (ALDH) 1A1 and anti-apoptotic Bcl-2, but increased pro-apoptotic Bax protein expression, leading to increases in residual EtOH concentration and the cellular oxidative stress marker, malondialdehyde. Ethanol 34-38 BCL2-associated X protein Mus musculus 192-195 33713693-10 2021 Ethanol exposure decreased cell viability and the expression of BDNF and increased the cell apoptosis rate and the expression of BAX, cleaved caspase-3, IL-1beta and IL-6. Ethanol 0-7 BCL2-associated X protein Mus musculus 129-132 29138110-3 2018 Wild-type and Bax knockout mice were given a pair of injections (two hours apart) of ethanol (2.5 g/kg) or saline on postnatal day (P) 4, P7, P10, or P13. Ethanol 85-92 BCL2-associated X protein Mus musculus 14-17 29138110-11 2018 Thus, ethanol-induced death of cortical neurons is Bax-dependent, occurs concurrently in all layers, but does not correspond to lamina- and age-dependent expression of DNA fragmentation. Ethanol 6-13 BCL2-associated X protein Mus musculus 51-54 27239851-3 2016 The influence of chronic ethanol consumption on the expression of the Bdnf, Bax, Bcl-xL, and CASP3 genes was studied in the brain structures of B6-1473C (C/C) and B6-1473G (G/G) mice that had been obtained on the base of the C57BL/6 strain. Ethanol 25-32 BCL2-associated X protein Mus musculus 76-79 27983966-11 2016 Moreover, increased cell apoptosis and pro-apoptotic protein Bax and caspase 3 were observed in ethanol treated mice, while the anti-apoptotic protein Bcl 2 was inhibited. Ethanol 96-103 BCL2-associated X protein Mus musculus 61-64