PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27771871-6 2017 Administration of either IPostC or CsA alone in nondiabetic animals significantly reduced CK, TNF-alpha, IL-1beta, and IL-6 concentrations, increased the p-GSK3beta and Bcl-2, and decreased the level of apoptosis (P < 0.05) but had no effect on diabetic hearts. Cyclosporine 35-38 BCL2, apoptosis regulator Rattus norvegicus 169-174 31654209-5 2020 In the presence of Ca2+, AGM also activated the Bcl-2 family protein Bax, a key factor in inducing MOMP, which is inactivated by CsA. Cyclosporine 129-132 BCL2, apoptosis regulator Rattus norvegicus 48-53 32569592-9 2020 In addition, exposure to CsA resulted in an increased expression of Bax, and a decreased expresion in that of Bcl-2, with a concomitant up-regulation of the Bax/Bcl-2, c-Caspase-3/p-Caspase-3 ratio and cytochrome c level. Cyclosporine 25-28 BCL2, apoptosis regulator Rattus norvegicus 110-115 32569592-9 2020 In addition, exposure to CsA resulted in an increased expression of Bax, and a decreased expresion in that of Bcl-2, with a concomitant up-regulation of the Bax/Bcl-2, c-Caspase-3/p-Caspase-3 ratio and cytochrome c level. Cyclosporine 25-28 BCL2, apoptosis regulator Rattus norvegicus 161-166 30725434-7 2019 CsA significantly decreased the Bax/Bcl-2 ratio, cl-casp-9/casp-9, and cl-casp-3/casp-3 in a concentration-dependent manner. Cyclosporine 0-3 BCL2, apoptosis regulator Rattus norvegicus 36-41 30121055-5 2018 Results: Our results showed that SC administration of CsA (30 mg/kg) to rats produced marked injury and apoptosis, elevation of Baxprotein expression, and inhibitionof Bcl-2protein expression in the kidneys, which were reversed significantly by oral administration of RG (0.2 or 0.4 mg/kg). Cyclosporine 54-57 BCL2, apoptosis regulator Rattus norvegicus 168-173 24508908-8 2014 CsA markedly decreased expressions of Nur77, p-Nur77, Bcl-2 and cyto C, and inhibited apoptosis.Improvement of neurological deficit, alleviation of brain edema and amelioration of EBI were obtained after prophylactic use of CsA. Cyclosporine 0-3 BCL2, apoptosis regulator Rattus norvegicus 54-59 25299210-12 2014 In conclusion, these results suggest that CsA induction of apoptotic or autophagic cell death in rat pituitary GH3 cells depends on the relative expression of factors and correlates with Bcl-2 and Mn-SOD levels. Cyclosporine 42-45 BCL2, apoptosis regulator Rattus norvegicus 187-192 27357441-4 2016 In addition, CsA treatment blocked the CoCl2-induced increases in ROS production and mitochondrial dysfunction, including a decrease in membrane potential, cytochrome c (cyto-c) release, Bax/Bcl-2 imbalance, as well as the ratios of cl-casp-9/casp-9 and cl-casp-3/casp-3 ratios, via the inhibition of p38 and ERK MAPK signaling pathways. Cyclosporine 13-16 BCL2, apoptosis regulator Rattus norvegicus 191-196 26844915-5 2016 Moreover, cyclosporine A significantly reduced serum albumin, creatinine clearance, urinary total antioxidant, superoxide dismutase, glutathione and Bcl2 protein levels. Cyclosporine 10-24 BCL2, apoptosis regulator Rattus norvegicus 149-153 26225924-8 2015 Also, a high protein expression of Bax with decreased Bcl-2 was revealed in the renal tissue of the CsA treated group. Cyclosporine 100-103 BCL2, apoptosis regulator Rattus norvegicus 54-59 25757124-11 2015 Expressions of Bcl-2, cleaved caspase 3, and cytoplasmic cytochrome C were significantly decreased in the CsA-treated groups compared with the control group. Cyclosporine 106-109 BCL2, apoptosis regulator Rattus norvegicus 15-20 24261911-7 2014 RESULTS: In CsA-treated rats, bcl-2 expression was significantly upregulated, whereas caspase-3 expression was downregulated, along with a reduced number of TUNEL-positive cells. Cyclosporine 12-15 BCL2, apoptosis regulator Rattus norvegicus 30-35 24261911-8 2014 The site-specific distribution of bcl-2 was consistent with the site-specific hyperplasia of the gingival epithelium in CsA-treated rats. Cyclosporine 120-123 BCL2, apoptosis regulator Rattus norvegicus 34-39 24261911-10 2014 The antiapoptotic protein bcl-2 might play a critical role in the pathogenesis of the site-specific hyperplasia of gingival epithelium induced by CsA. Cyclosporine 146-149 BCL2, apoptosis regulator Rattus norvegicus 26-31 23160799-10 2013 Dvl-1 down-regulation decreased the apoptotic rate, caspase-3 activity, and the Bax/Bcl-2 ratio in H9c2 cells treated with CsA. Cyclosporine 123-126 BCL2, apoptosis regulator Rattus norvegicus 84-89 23595141-6 2013 Both diazoxide and cyclosporin A exerted significant protective effects on cell viability by ameliorating the decrease in Bcl-2 and the increase in cytochrome c and caspase-3 activity induced by A-beta1-42. Cyclosporine 19-32 BCL2, apoptosis regulator Rattus norvegicus 122-127 23683031-10 2013 CsA increased the protein expression of bax, cleaved caspase-9, caspase-3 and the activity of caspase-3; however, the anti-apoptotic bcl-2 protein was reduced. Cyclosporine 0-3 BCL2, apoptosis regulator Rattus norvegicus 133-138 23498817-7 2013 In addition, emodin prevented increased Bax/Bcl-2 ratio induced by CsA. Cyclosporine 67-70 BCL2, apoptosis regulator Rattus norvegicus 44-49 23160799-12 2013 Moreover, we further deleted the downstream member beta-catenin by specific siRNA, and found that CsA-induced the Bax/Bcl-2 ratio and the expression of c-Myc, which were attenuated. Cyclosporine 98-101 BCL2, apoptosis regulator Rattus norvegicus 118-123 21310770-7 2011 RESULTS: Compared with the control group, acidic buffer or plus cyclosporine A post-conditioning significantly improved myocardial performance, decreased cytochrome C release into the cytosol, increased Bcl-2 expression and decreased Bax expression, decreased sensitivity of mPTP-opening to [Ca2+] and the rate of apoptosis after reperfusion. Cyclosporine 64-78 BCL2, apoptosis regulator Rattus norvegicus 203-208 23258196-12 2013 RUS decreased CsA-induced increased expression of Bax/Bcl-2 ratio. Cyclosporine 14-17 BCL2, apoptosis regulator Rattus norvegicus 54-59 21776863-0 2011 [Apoptosis and expression of Bcl-2 and caspase-3 in ciclosporin-induced gingival overgrowth of rats]. Cyclosporine 52-63 BCL2, apoptosis regulator Rattus norvegicus 29-34 21776863-1 2011 OBJECTIVE: To observe the effect of Ciclosporin (CsP) on apoptosis and expression of the associated protein Bcl-2, Caspase-3 in gingival epithelium of rats in order to approach the mechanism of CsP-induced gingival epithelium overgrowth. Cyclosporine 36-47 BCL2, apoptosis regulator Rattus norvegicus 108-113 22678567-5 2012 H9c2 cells were treated with CsA in a dose-dependent manner, and decreased Bcl-2 expression, increased Bax expression, and caspase-3 activation were observed. Cyclosporine 29-32 BCL2, apoptosis regulator Rattus norvegicus 75-80 21490080-7 2011 RESULTS: Compared with the control group, acidic buffer or plus cyclosporine A post-conditioning significantly improved myocardial performance, decreased cytochrome C release into the cytosol, increased Bcl-2 expression and decreased Bax expression, decreased sensitivity of mPTP-opening to [Ca2+] and the rate of apoptosis after reperfusion. Cyclosporine 64-78 BCL2, apoptosis regulator Rattus norvegicus 203-208 16980052-8 2006 Pro-caspase-3 and Bcl-2 proteins were decreased by CsA. Cyclosporine 51-54 BCL2, apoptosis regulator Rattus norvegicus 18-23 16980055-12 2006 RMCs with CsA reduced Bcl-2 and cIAP expression. Cyclosporine 10-13 BCL2, apoptosis regulator Rattus norvegicus 22-27 16980055-13 2006 CONCLUSIONS: In this study, CsA induced apoptosis by up-regulating proapoptotic factors, caspase-3 and -6, p53, Bax, cleaving PARP, and down-regulating antiapoptotic factor, Bcl-2, and cIAP. Cyclosporine 28-31 BCL2, apoptosis regulator Rattus norvegicus 174-179 15147634-6 2004 Bcl-2 expression increased significantly in neurons after 14 and even more after 21 days of treatment with 7 mg/kg cyclosporine-A, mainly in type B and C neurons. Cyclosporine 115-129 BCL2, apoptosis regulator Rattus norvegicus 0-5 15784653-13 2005 In general, WW85 had no direct action on expression of the proapoptotic gene, Fas ligand; however, WW85 given alone or with cyclosporine enhanced expression of antiapoptotic genes Bcl-2 and Bcl-xL. Cyclosporine 124-136 BCL2, apoptosis regulator Rattus norvegicus 180-185 15614148-5 2004 RESULTS: CsA-induced tubular cell apoptosis; cellular infiltration; and increase of Fas, Bax, TGF-beta protein expression with significant tubulointerstitial fibrosis, and reduced Bcl2 protein expression. Cyclosporine 9-12 BCL2, apoptosis regulator Rattus norvegicus 180-184 15614148-7 2004 CONCLUSIONS: These findings suggest that chronic CsA nephrotoxicity is related to Bax and Bcl2-related apoptosis pathways, and that alpha-MSH can attenuate the CsA-induced tubulointerstitial fibrosis as well as tubular cell apoptosis. Cyclosporine 49-52 BCL2, apoptosis regulator Rattus norvegicus 90-94 15746540-7 2005 Increased apoptotic cell death in CsA-treated rat kidneys was significantly decreased with rHuEPO cotreatment, and apoptosis-related genes were regulated in favor of cell survival (increased Bcl-2 and suppressed caspase-3). Cyclosporine 34-37 BCL2, apoptosis regulator Rattus norvegicus 191-196 15147634-7 2004 With 15 mg/kg cyclosporine-A, Bcl-2 increased moderately in type A and B neurons and strongly in type C neurons only after 7 days. Cyclosporine 14-28 BCL2, apoptosis regulator Rattus norvegicus 30-35 15147634-10 2004 We conclude that (1) in normal conditions, Bax and Bcl-2 were differently expressed in neurons and satellite cells; (2) cyclosporine-A treatment rapidly enhanced Bax expression in satellite cells only, whereas Bcl-2 expression increased moderately in type A neurons and was strongly expressed in type B and C neurons; (3) cyclosporine-A has a protective role in neurons but not in satellite cells; and (4) the neuroprotective role of cyclosporine-A is dose dependent. Cyclosporine 120-134 BCL2, apoptosis regulator Rattus norvegicus 51-56 15147634-10 2004 We conclude that (1) in normal conditions, Bax and Bcl-2 were differently expressed in neurons and satellite cells; (2) cyclosporine-A treatment rapidly enhanced Bax expression in satellite cells only, whereas Bcl-2 expression increased moderately in type A neurons and was strongly expressed in type B and C neurons; (3) cyclosporine-A has a protective role in neurons but not in satellite cells; and (4) the neuroprotective role of cyclosporine-A is dose dependent. Cyclosporine 120-134 BCL2, apoptosis regulator Rattus norvegicus 210-215 12066135-8 2002 The decreased expression of Bcl-2 and the ratio of Bcl-2 to Bax protein seen in cyclosporine-treated rat kidneys were significantly increased after colchicine treatment, accompanying a suppression of caspase-3 activity (P <.05). Cyclosporine 80-92 BCL2, apoptosis regulator Rattus norvegicus 28-33 12066135-8 2002 The decreased expression of Bcl-2 and the ratio of Bcl-2 to Bax protein seen in cyclosporine-treated rat kidneys were significantly increased after colchicine treatment, accompanying a suppression of caspase-3 activity (P <.05). Cyclosporine 80-92 BCL2, apoptosis regulator Rattus norvegicus 51-56 10594790-11 1999 CsA induced the expression of p53 (P < 0.05) and Bax (P < 0.01) and decreased that of Bcl-2 (P < 0.05). Cyclosporine 0-3 BCL2, apoptosis regulator Rattus norvegicus 92-97 10942734-3 2000 The resting DeltaPsi of Bcl-2 nonexpressing PC12 and wild-type SY5Y cells was increased significantly by the presence of the PTP inhibitor cyclosporin A (CsA) or by intracellular Ca(2+) chelation through exposure to the acetoxymethyl ester of 1, 2-bis(2-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid (BAPTA-AM). Cyclosporine 154-157 BCL2, apoptosis regulator Rattus norvegicus 24-29