PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23843283-6 2013 The number of c-Jun and Bcl-2 positive motoneurons was increased immediately after avulsion both in control and VPA group, however, the percent of c-Jun positive motoneurons was decreased and the percent of Bcl-2 positive motoneurons was increased by VPA treatment significantly. Valproic Acid 112-115 BCL2, apoptosis regulator Rattus norvegicus 24-29 25206605-5 2013 Results showed that valproic acid significantly increased the expression of Bcl-2 and growth associated protein 43, and reduced the c-Jun expression after brachial plexus avulsion. Valproic Acid 20-33 BCL2, apoptosis regulator Rattus norvegicus 76-81 21036453-11 2011 Anti-apoptotic Bcl-2 protein markedly increased after 6 (p=0.04) and 24h (p=0.014) of VPA treatment. Valproic Acid 86-89 BCL2, apoptosis regulator Rattus norvegicus 15-20 15872096-2 2005 A series of microarray studies with validating criteria have recently revealed a common, novel target for the long-term actions of the structurally highly dissimilar mood stabilizers lithium and valproate: BAG-1 [BCL-2 (B-cell CLL/lymphoma 2)-associated athanogene]. Valproic Acid 195-204 BCL2, apoptosis regulator Rattus norvegicus 213-218 18656628-9 2008 CONCLUSION: VPA treatment acetylates H3K9 and beta-catenin and enhances translocation of beta-catenin into the nucleus, where it colocalizes with Ac-H3K9 and stimulates the transcription of survival gene bcl-2. Valproic Acid 12-15 BCL2, apoptosis regulator Rattus norvegicus 204-209 18496777-2 2008 It has recently been demonstrated that VPA could promote neurite outgrowth, activate the extracellular signal-regulated kinase pathway, and increase B-cell lymphoma/leukemia-2 (bcl-2)and growth cone-associated protein 43 (GAP-43) levels in spinal cord. Valproic Acid 39-42 BCL2, apoptosis regulator Rattus norvegicus 177-182 15379904-8 2004 Valproate also regulated the expression of survival genes, Bad and Bcl-2, at different times of treatment. Valproic Acid 0-9 BCL2, apoptosis regulator Rattus norvegicus 67-72 29957469-4 2018 We found that VPA effectively prevented Abeta25-35-stimulated cytotoxicity through attenuating apoptosis and increasing the ratio of Bcl-2/Bax in PC12 cells. Valproic Acid 14-17 BCL2, apoptosis regulator Rattus norvegicus 133-138 12559103-6 2003 Supporting this possibility are recent findings that chronic treatment with valproate increased the expression of endoplasmic reticulum stress protein GRP78 and antiapoptotic factor bcl-2 in rat cerebral cortex. Valproic Acid 76-85 BCL2, apoptosis regulator Rattus norvegicus 182-187 12559103-7 2003 Since GRP78 binds Ca(2+) and folds damaged protein, bcl-2 stabilizes mitochondrial transmembrane potential and inhibits cytochrome C release, and both GRP78 and bcl-2 have been shown to inhibit oxyradical accumulation, together these findings indicate that valproate may target one or more of these processes in order to produce neuroprotective effects. Valproic Acid 257-266 BCL2, apoptosis regulator Rattus norvegicus 52-57 12559103-7 2003 Since GRP78 binds Ca(2+) and folds damaged protein, bcl-2 stabilizes mitochondrial transmembrane potential and inhibits cytochrome C release, and both GRP78 and bcl-2 have been shown to inhibit oxyradical accumulation, together these findings indicate that valproate may target one or more of these processes in order to produce neuroprotective effects. Valproic Acid 257-266 BCL2, apoptosis regulator Rattus norvegicus 161-166 32825436-9 2020 Moreover, VPA increased the gene expression of an apoptotic marker, caspase-3, with a decrease in anti-apoptotic Bcl2 and nuclear factor erythroid 2-related factor 2 (Nrf2) transcriptional factor. Valproic Acid 10-13 BCL2, apoptosis regulator Rattus norvegicus 113-117 32825436-11 2020 CONCLUSION: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2. Valproic Acid 39-42 BCL2, apoptosis regulator Rattus norvegicus 233-238 15269271-6 2004 We found that chronic treatment of rats with valproate increased levels of activated phospho-ERK44/42 in neurons of the anterior cingulate, a region in which we found valproate-induced increases in expression of an ERK pathway-regulated gene, bcl-2. Valproic Acid 45-54 BCL2, apoptosis regulator Rattus norvegicus 243-248 15269271-6 2004 We found that chronic treatment of rats with valproate increased levels of activated phospho-ERK44/42 in neurons of the anterior cingulate, a region in which we found valproate-induced increases in expression of an ERK pathway-regulated gene, bcl-2. Valproic Acid 167-176 BCL2, apoptosis regulator Rattus norvegicus 243-248 15013030-1 2004 Recent studies in rat brain and cell cultures have demonstrated that expression of the peptide-folding chaperone protein calreticulin is increased by valproate treatment, while the anti-apoptotic Bcl-2 is increased by both lithium and valproate. Valproic Acid 235-244 BCL2, apoptosis regulator Rattus norvegicus 196-201 34217161-0 2021 Valproic Acid Ameliorates Locomotor Function in the Rat Model of Contusion via Alteration of Mst1, Bcl-2, and Nrf2 Gene Expression. Valproic Acid 0-13 BCL2, apoptosis regulator Rattus norvegicus 99-104 32901855-9 2020 Notably, HG markedly promoted apoptosis of NRK-52E cells by regulating the protein levels of Bax, cleaved caspase-3 and Bcl-2, which was attenuated by simultaneous VPA treatment. Valproic Acid 164-167 BCL2, apoptosis regulator Rattus norvegicus 120-125 29198746-8 2017 Consistent with the TUNEL staining, VPA administration also obviously suppressed the ratio of Bax: Bcl-2 and the expression of cleaved caspase-3 and PARP in optic nerve in EAE rats. Valproic Acid 36-39 BCL2, apoptosis regulator Rattus norvegicus 99-104 26639559-3 2016 We found that DHA supplementation (75, 150 or 300 mg/kg/day, 21 days) rescued the VPA (600 mg/kg) induced DHA reduction in plasma and hippocampus in a dose-dependent manner, increased the levels of hippocampal p-CaMKII and p-CREB without affecting total protein level, and altered BDNF-AKT-Bcl-2 signaling pathway, as well as inhibited the activity of caspase-3. Valproic Acid 82-85 BCL2, apoptosis regulator Rattus norvegicus 290-295 28803955-4 2017 In this study, we investigated the alteration of Bcl-2 level and associated mechanisms in valproic acid (VPA) exposed ASD rats. Valproic Acid 90-103 BCL2, apoptosis regulator Rattus norvegicus 49-54 28803955-4 2017 In this study, we investigated the alteration of Bcl-2 level and associated mechanisms in valproic acid (VPA) exposed ASD rats. Valproic Acid 105-108 BCL2, apoptosis regulator Rattus norvegicus 49-54 26886004-0 2016 Valproic acid-mediated myocardial protection of acute hemorrhagic rat via the BCL-2 pathway. Valproic Acid 0-13 BCL2, apoptosis regulator Rattus norvegicus 78-83 26886004-9 2016 Increased expression of BCL-2 messenger RNA was observed following VPA treatment in the heart tissues of hemorrhagic rats (approximately 4.9-fold) and in H9c2 cells that survived CoCl2-induced hypoxia (approximately 4.9-fold). Valproic Acid 67-70 BCL2, apoptosis regulator Rattus norvegicus 24-29 26886004-10 2016 Western blot analysis showed a concomitant increase in BCL-2 protein expression and Akt phosphorylation following VPA treatment. Valproic Acid 114-117 BCL2, apoptosis regulator Rattus norvegicus 55-60 26886004-12 2016 CONCLUSION: These findings suggest that VPA protects myocardial cells from hemorrhagic and hypoxic stress through the Akt/BCL-2 survival pathway, indicating a potential use of HDACIs for acute severe hemorrhage treatment. Valproic Acid 40-43 BCL2, apoptosis regulator Rattus norvegicus 122-127 28803955-0 2017 Valproic acid exposure decreases the mRNA stability of Bcl-2 via up-regulating miR-34a in the cerebellum of rat. Valproic Acid 0-13 BCL2, apoptosis regulator Rattus norvegicus 55-60 28646254-12 2017 Furthermore, VP-treated animals exhibited high immunoexpression of Bax protein and increased levels of Bax and caspase-3 while level of Bcl2 was significantly decreased in hepatic tissue. Valproic Acid 13-15 BCL2, apoptosis regulator Rattus norvegicus 136-140 29938967-0 2015 Neuroprotective action of valproic acid accompanied of the modification on the expression of Bcl-2 and activated caspase-3 in the brain of rats submitted to ischemia/reperfusion. Valproic Acid 26-39 BCL2, apoptosis regulator Rattus norvegicus 93-98 29938967-6 2015 Besides, it was found by westernblot, that in homogenized brain tissue of the animals under ischemia-reperfusion which receivedvalproic acid, there was a rise on the density of the bands corresponding to Bcl-2, and a reductionof activated 3-capase in comparison to the ones who were not treated with the antiepileptic drug.It"s concluded that the treatment with valproic acid prevented the neurological deficit in healthyrats under Ischemia-reperfusion, blocking the effect of free radicals on lipids and proteins ofthe affected brain cortex, and it is suggested that the same drug intervenes on apoptosis inducedduring this type of damage, being able to be a therapeutic alternative in the treatment of cerebralischemia. Valproic Acid 127-140 BCL2, apoptosis regulator Rattus norvegicus 204-209