PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27861627-4 2016 Z-VAD-FMK prevented caspase-3 activation and apoptosis and decreased BNIP-3 (Bcl-2/adenovirus E1B 19-kDa interacting protein 3) expression levels and apoptosis-inducing factor/endonuclease G (AIF/Endo G) translocation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 3 Rattus norvegicus 20-29 29317206-8 2018 We found that exendin-4 can decrease the AR42J cell viability as well as increase the cell death and cleaved caspase-3 level, which all can be inhibited by z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 156-165 caspase 3 Rattus norvegicus 109-118 27255381-8 2016 Doxorubicin also induced caspase-3 and -7 activity in INS-1 832/13 cells and mouse islets; co-treatment with the pan-caspase inhibitor Z-VAD-FMK temporarily attenuated the doxorubicin-mediated loss of viability in INS-1 832/13 cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 135-144 caspase 3 Rattus norvegicus 25-41 26526840-7 2016 We also found that caspase-3 activation was a downstream event of PARP activation and that apoptosis of MCs was suppressed, although not completely, by pretreatment with the pan-caspase inhibitor z-VAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 196-205 caspase 3 Rattus norvegicus 19-28 27324074-9 2016 Pretreatment with zVAD-fmk significantly inhibited a post-SAP increase in the activation of MPO, TNF-alpha, IL-1beta, and caspase-3, and decreased lung injury induced by SAP as determined by the pathologic score. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 18-26 caspase 3 Rattus norvegicus 122-131 24939579-9 2014 Inhibition of caspase induced by z-VAD-fmk reduced the expression and activation of caspase-3, -8 and -9 (P<0.01). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 33-42 caspase 3 Rattus norvegicus 84-104 26699793-6 2015 The cardioprotective roles of SP2 were partly resulted from the downregulated expression and activity of caspase-3 in which the effect was similar to the caspase inhibitor, z-VAD-fmk, and could be rescued by caspase activator, PAC-1. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 173-182 caspase 3 Rattus norvegicus 105-114 20422475-8 2011 The action of PACAP was mimicked by D-JNKi1 and Z-VAD-FMK, indicating the involvement of the jun and caspase-3 pathways in alcohol toxicity. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 48-57 caspase 3 Rattus norvegicus 101-110 24396410-7 2014 The caspase inhibitor z-VAD-fmk reduced the expression and activation of caspase-3, caspase-8 and caspase-9 in the irradiated rats, indicating that caspase may be a potential therapeutic target in the treatment of brain radiation injury. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 22-31 caspase 3 Rattus norvegicus 73-82 24314135-12 2013 Caspase-3 activity and its inhibition by Z-VAD-fmk were measured by caspase-3 fluorometric assay. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 41-50 caspase 3 Rattus norvegicus 0-9 21138749-5 2011 Although partially blocked by Z-VAD-fmk, this effect was coincident to caspase-3 activation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 30-39 caspase 3 Rattus norvegicus 71-80 14559356-4 2003 EGCG or z-VAD-fmk-pretreated PC12 cells showed an increase of viability compared to untreated PC12 cells, and pretreatment of PC12 cells with either agent induced a dose-dependent inhibition of caspase-3 activation and PARP cleavage. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 8-17 caspase 3 Rattus norvegicus 194-203 19082426-5 2008 Significant increased numbers of caspase-positive cells were observed by anti-caspase 3 immunolabeling after instillation of ANG (P<0.01); the same doses of LOS or ZVAD-fmk that blocked TUNEL also blocked the activation of caspase 3 (P<0.01). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 167-175 caspase 3 Rattus norvegicus 226-235 17432720-11 2007 A significant increase in the cytosolic expression of active caspase-3 was evident 24 hours after high-overpressure shock wave application; this increase was prevented by Z-VAD-FMK administration. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 171-180 caspase 3 Rattus norvegicus 61-70 17292420-17 2007 Z-VAD-fmk indeed inhibited the caspase-3 activation in intestinal mucosa of SAP. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 3 Rattus norvegicus 31-40 17325185-15 2007 The z-VAD-fmk inhibitor blocked caspase-3 activities in the homogeneous ARPE-19 cultures but not in the heterogeneous R28 cultures. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 4-13 caspase 3 Rattus norvegicus 32-41 16733814-10 2006 Inhibition of caspase-3 activation by inhibitor (z-VAD-fmk) completely blocked DADS-induced apoptosis on N18 cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 49-58 caspase 3 Rattus norvegicus 14-23 14988591-6 2004 B-D-FMK (40 microM), Z-DEVD-FMK (15 microM) and Z-VAD-FMK (22 microM) almost completely inhibited the 25-fold increase in Caspase-3 activity and decreased apoptosis from 15.9 +/- 4.4 to 2.0 +/- 0.6% (p < 0.01), 15.0 +/- 2.2 and 15.0 +/- 2.2% respectively. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 48-57 caspase 3 Rattus norvegicus 122-131 14622126-5 2003 Caspase-3 activity increased with a delay of more than 10 h following cessation of the heat stress, reaching a peak at approximately 18 h. Neuronal death measured 1-3 days after the stress was reduced by the general caspase inhibitors qVD-OPH (10-20 microm) and zVAD-fmk (50-100 microm). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 262-270 caspase 3 Rattus norvegicus 0-9 20371263-12 2010 Either antioxidant tempol or a pancaspase inhibitor Z-VAD-FMK decreased cell death as well as caspase 3/7 activity induced by SLD sulfide/TNF coexposure. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 52-61 caspase 3 Rattus norvegicus 94-103 16344902-8 2005 Both a broad-spectrum caspase inhibitor Z-VAD-FMK (50 mumol/L) and a specific caspase-3 inhibitor Z-DEVD-FMK (100 micromol/L) increased viable PC12 cells to 45.16%, (Z-DEVD-FMK) and 58.06%, (Z-VAD-FMK), respectively, in the presence of roscovitine. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 191-200 caspase 3 Rattus norvegicus 78-87 15322302-7 2004 z-VAD-FMK suppressed TUNEL and caspase-3 staining in endothelial cells, decreased caspase-3 activation, reduced BBB permeability, relieved vasospasm, abolished brain edema, and improved neurological outcome. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 3 Rattus norvegicus 31-40 15322302-7 2004 z-VAD-FMK suppressed TUNEL and caspase-3 staining in endothelial cells, decreased caspase-3 activation, reduced BBB permeability, relieved vasospasm, abolished brain edema, and improved neurological outcome. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-9 caspase 3 Rattus norvegicus 82-91 15183012-5 2004 Also, dieldrin (30-300 microM) treatment induced proteolytic cleavage of poly(ADP-ribose) polymerase (PARP), which was blocked by pretreatment with caspase-3 inhibitors Z-DEVD-FMK and Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 184-193 caspase 3 Rattus norvegicus 148-157 9467964-8 1998 The activation of CPP32 and apoptotic cell death were inhibited by addition of Z-VAD-fmk, a universal inhibitor of ICE-like proteases. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 79-88 caspase 3 Rattus norvegicus 18-23 12623880-11 2003 The 24-hour cotreatment with z-VAD-fmk effectively prevented losartan-induced caspase-3 activation and internucleosomal DNA fragmentation, as well as SMC depletion and the reductions in aortic mass and DNA content. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 29-38 caspase 3 Rattus norvegicus 78-87 12208500-4 2002 Experiments with iodotubercidin, dicoumarol and z-VAD-fmk, which inhibited AMPK, JNK and caspase activation, respectively, supported the notion that prolonged AMPK activation in liver cells induces apoptosis through an activation pathway that involves JNK and caspase-3. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 48-57 caspase 3 Rattus norvegicus 260-269 11511102-3 2001 In Rat-1 cells, cleavage of paxillin by caspase-3 was suppressed by zVAD-fmk or zDEVD-cmk, making caspase-3 a likely executioner during etoposide-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 68-76 caspase 3 Rattus norvegicus 40-49 11511102-3 2001 In Rat-1 cells, cleavage of paxillin by caspase-3 was suppressed by zVAD-fmk or zDEVD-cmk, making caspase-3 a likely executioner during etoposide-induced apoptosis. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 68-76 caspase 3 Rattus norvegicus 98-107 11006098-4 2000 On the other hand, zVAD-fmk did not inhibit the mitochondrial event such as the reduction of the mitochondrial membrane potential and cytochrome c release although it prevented caspase-3 activation, nuclear condensation, and DNA fragmentation. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 19-27 caspase 3 Rattus norvegicus 177-186 10778806-7 2000 Ceramide-induced RPE cell death was inhibited by zVAD-fmk, a CPP32-like protease inhibitor. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 49-57 caspase 3 Rattus norvegicus 61-66 12675269-10 2003 Using the caspase-inhibitors ac-IEPD-CHO, ac-DEVD-CHO and zVAD-fmk, it was shown that inhibition of the effector caspase-3 prevented A-NK cell induced apoptosis in CC531-bcl-2 cells, but not in CC531s cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 58-66 caspase 3 Rattus norvegicus 113-122 11850844-5 2002 In MT-450 mammary carcinoma cells hyperforin increased the activity of caspase-9 and caspase-3, and hyperforin-mediated apoptosis was blocked by the broad-range caspase inhibitor zVAD.fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 179-183 caspase 3 Rattus norvegicus 85-94 11003619-9 2000 However, recruitment and processing of caspases-3 and -7 were prevented by Z-VAD.FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 75-84 caspase 3 Rattus norvegicus 39-56 11045015-4 2000 The inhibitory peptide relatively specific for caspase-3, z-DEVD-FMK and non-selective caspase inhibitor z-VAD-FMK inhibited activation of caspase-3 and apoptotic cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 105-114 caspase 3 Rattus norvegicus 139-148 10940360-6 2000 zVAD treatment significantly decreased the levels of caspases 3, 8 and 9 but did not provide neuroprotection for the cholinergic neurons. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-4 caspase 3 Rattus norvegicus 53-72 8940042-6 1996 In living cells, zVAD-FMK, a pseudosubstrate aspartase inhibitor, blocked the activity/activation of the aspartase at concentrations about one order of magnitude lower than those required to promote survival, raising the possibility that the CPP32-like aspartase is not the main death effector in this model. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 17-25 caspase 3 Rattus norvegicus 242-247