PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32986023-6 2020 Bath application of glutamate to midbrain cultures causes abnormal elevations in intracellular Ca2+ within neurons and this is accompanied by caspase-3 activation in DA neurons, as demonstrated by immunostaining. Glutamic Acid 20-29 caspase 3 Mus musculus 142-151 34044281-0 2021 Neuroprotective effects of Senkyunolide I against glutamate-induced cells death by attenuating JNK/caspase-3 activation and apoptosis. Glutamic Acid 50-59 caspase 3 Mus musculus 99-108 34044281-12 2021 Our findings demonstrate that SEI protected Neuro2a cells against glutamate toxicity by regulating JNK/caspase-3 pathway and apoptosis. Glutamic Acid 66-75 caspase 3 Mus musculus 103-112 30878614-3 2019 In L-glutamic acid (L-Glu)-damaged HT22 cells, a 3-h pre-incubation with IOPS enhanced cell viability, inhibited apoptosis and caspase-3 activity, reduced the release of lactate dehydrogenase, restored the dissipated mitochondrial membrane potential, and suppressed the excess accumulation of intracellular reactive oxygen species. Glutamic Acid 20-25 caspase 3 Mus musculus 127-136 32784451-4 2020 In the L-glutamate (L-Glu)-induced apoptosis of HT22 cells, IFY increased cell viability, inhibited mitochondrial apoptosis, and reduced the intracellular levels of reactive oxygen species (ROS), caspase-3, -8 and -9 after 3 h of pretreatment and 12-24 h of co-incubation. Glutamic Acid 7-18 caspase 3 Mus musculus 196-216 32784451-4 2020 In the L-glutamate (L-Glu)-induced apoptosis of HT22 cells, IFY increased cell viability, inhibited mitochondrial apoptosis, and reduced the intracellular levels of reactive oxygen species (ROS), caspase-3, -8 and -9 after 3 h of pretreatment and 12-24 h of co-incubation. Glutamic Acid 20-25 caspase 3 Mus musculus 196-216 28477054-0 2018 Neuroprotective Effects of Sigesbeckia pubescens Extract on Glutamate-Induced Oxidative Stress in HT22 Cells via Downregulation of MAPK/caspase-3 Pathways. Glutamic Acid 60-69 caspase 3 Mus musculus 136-145 29588166-5 2018 The results showed that BHAPI significantly increased cell viability, decreased lactate dehydrogenase (LDH) release, inhibited apoptotic cell death and reduced the activation of caspase-3 after glutamate treatment. Glutamic Acid 194-203 caspase 3 Mus musculus 178-187 30221730-4 2018 In L-Glu-damaged HT22 cells, SC significantly increased cell viability, inhibited lactate dehydrogenase release, reduced caspase-3 activity and suppressed apoptosis, which were determined via an MTT assay, an in vitro Toxicology Assay kit, a Caspase-3 activity assay kit, and propidium iodide and Annexin V staining. Glutamic Acid 3-8 caspase 3 Mus musculus 242-251 27151150-9 2016 Exposure of glutamate-treated cells to emodin induced an increase in the level of Bcl-2 expression, whereas the expression of Bax and active caspase-3 proteins was significantly reduced. Glutamic Acid 12-21 caspase 3 Mus musculus 141-150 27939422-7 2017 THSG inhibited generation of reactive oxygen species (ROS), expression of heme oxygenase-1, and activation of caspase-3 and calpain-1 proteases, all of which were increased by glutamate. Glutamic Acid 176-185 caspase 3 Mus musculus 110-119 28817120-8 2017 Consistent with this effect, MK-X significantly decreased caspase-3 cleavage and nuclear translocation of apoptosis-inducing factor induced by glutamate. Glutamic Acid 143-152 caspase 3 Mus musculus 58-67 27635193-8 2016 ClC-2 overexpression increased the expression of Bcl-2, decreased the expression of Bax, and decreased caspase-3 and -9 activation in RGC-5 cells treated with glutamate, but silencing of ClC-2 produced opposite effects. Glutamic Acid 159-168 caspase 3 Mus musculus 103-119 26187689-11 2015 (Val8)GLP-1-glu-PAL showed good effects in preventing the MPTP-induced motor impairment (Rotarod, open field locomotion, swim test), reduction in tyrosine hydroxylase levels (dopamine synthesis) in the substantia nigra, a reduction of activated caspase 3 levels, of TUNEL positive cell numbers, of the pro-apoptotic signaling molecule BAX and an increase in the growth signaling molecule Bcl-2. Glutamic Acid 12-15 caspase 3 Mus musculus 245-254 20623531-7 2010 In addition, we found that glutamate treatment decreased XIAP expression and increased caspase-3 activity in mtSOD1 cells and mIkappaBalpha-overexpressing wtSOD1 cells. Glutamic Acid 27-36 caspase 3 Mus musculus 87-96 24633087-9 2014 Furthermore, the addition of 9 mug/mL CSA to 10 mM glutamate significantly reduced caspase 3/7 activity by 1.3-fold (P<0.0005) and the amount of Annexin V+/PI- cells by 2.8-fold compared with RGC-5 cells incubated with 10 mM glutamate alone. Glutamic Acid 51-60 caspase 3 Mus musculus 83-92 24378639-9 2014 Glutamate treatment induced the loss of BV-2 cell viability, which was associated with an increase in the apoptotic rate, as well as an increase in the Bax/Bcl-2 ratio and the extracellular levels of cleaved caspase-3. Glutamic Acid 0-9 caspase 3 Mus musculus 208-217 23306786-7 2013 RESULTS: Under excitotoxic conditions (10 mM and 12 mM glutamate) RGC-5 cells incubated in SIS showed a statistically significant reduction in cell viability, cell amount, cell survival and caspase 3/7 activity compared to DMEM. Glutamic Acid 55-64 caspase 3 Mus musculus 190-199 21858143-9 2011 PRINCIPAL FINDINGS: As expected Glu treatment increased caspase 3 activity and cell death in the GT1-7 cells, but Glu alone did not induce cell death or affect caspase 3 activity in the SCN2.2 cells. Glutamic Acid 32-35 caspase 3 Mus musculus 56-65 20623531-8 2010 Our results suggest that glutamate excitotoxicity in motor neurons of SOD1-linked fALS is attributable, at least in part, to the impairment of IkappaBalpha-dependent RelA activation and subsequent apoptosis mediated by XIAP inhibition and caspase-3 activation. Glutamic Acid 25-34 caspase 3 Mus musculus 239-248 21113491-2 2010 Afobazole in a final concentration of 10(-8) M inhibits hyperactivation of effector apoptotic caspase-3 in HT-22 cell culture under conditions of glutamate toxicity. Glutamic Acid 146-155 caspase 3 Mus musculus 94-103 18296662-6 2008 Caspase-3 activation after glutamate treatment was determined with a carboxyfluorescein caspase-3 detection kit. Glutamic Acid 27-36 caspase 3 Mus musculus 0-9 18296662-6 2008 Caspase-3 activation after glutamate treatment was determined with a carboxyfluorescein caspase-3 detection kit. Glutamic Acid 27-36 caspase 3 Mus musculus 88-97 18296662-12 2008 Glutamate-mediated cell death involved activation of caspase-3, and sigma-1 receptor activation prevented an increase in caspase-3 expression. Glutamic Acid 0-9 caspase 3 Mus musculus 53-62 18296662-12 2008 Glutamate-mediated cell death involved activation of caspase-3, and sigma-1 receptor activation prevented an increase in caspase-3 expression. Glutamic Acid 0-9 caspase 3 Mus musculus 121-130 17973977-2 2008 Stimulation with glutamate or 6-hydroxy-dopamine caused activation of caspase-3 and apoptotic neuronal death which were both attenuated by JNK-inhibition. Glutamic Acid 17-26 caspase 3 Mus musculus 70-79 17261353-3 2007 Glutamate (1 mM) enhanced caspase-3 activity and lactate dehydrogenase (LDH) release in the hippocampal, neocortical and cerebellar neurons in time-dependent manner, and these data were confirmed at the cellular level with Hoechst 33342 and calcein AM staining. Glutamic Acid 0-9 caspase 3 Mus musculus 26-35 16776830-3 2006 RESULTS: Glutamate-induced apoptotic cell death in neuronal cells was associated with characteristic DNA fragmentation, morphological changes, activation of calpain and caspase-3 as well as the upregulation and/or translocation of AIF from mitochondria into cytosol and nuclei. Glutamic Acid 9-18 caspase 3 Mus musculus 169-178 17261757-2 2006 Glutamate-induced apoptosis is also associated with intracellular [Ca(2+)]i overload, generation of reactive oxygen species (ROS), depression of cell energy metabolism, cytochrome c release, and increase in caspase-3 activity. Glutamic Acid 0-9 caspase 3 Mus musculus 207-216 16776830-5 2006 In primary cortical cells, glutamate induces activation of calpain, caspase-3 and translocation of AIF from mitochondria to cytosol and nuclei. Glutamic Acid 27-36 caspase 3 Mus musculus 68-77 16776830-8 2006 CONCLUSION: Depending upon the neuronal cell type, at least two mechanisms are involved in glutamate-induced apoptosis: a caspase-3-dependent pathway and a caspase-independent pathway involving calpain and AIF. Glutamic Acid 91-100 caspase 3 Mus musculus 122-131 16776830-10 2006 Kinetics of this apoptotic pathway further indicate that calpain rather than caspase-3, plays a critical role in the glutamate-induced apoptosis. Glutamic Acid 117-126 caspase 3 Mus musculus 77-86 16515537-3 2006 We found that the compounds similarly inhibit free-radical generation in an abiotic system, as well as indices of neurotoxicity (caspase-3 activity and lactate dehydrogenase release) induced by glutamate in mouse embryonic primary cell cultures (a preparation resistant to NMDA toxicity). Glutamic Acid 194-203 caspase 3 Mus musculus 129-138 16371440-4 2006 In cerebral endothelial cells, glutamate (0.1-2.0 mM) increased formation of reactive oxygen species, including superoxide radicals, and induced major keystone events of apoptosis, such as NF-kappaB nuclear translocation, caspase-3 activation, DNA fragmentation, and cell detachment. Glutamic Acid 31-40 caspase 3 Mus musculus 222-231 16567804-9 2006 Taken together, our findings suggest that caspase-3 cleavage of EAAT2 is one mechanism responsible for the impairment of glutamate uptake in mutant SOD1-linked ALS. Glutamic Acid 121-130 caspase 3 Mus musculus 42-51 10321830-6 1999 This protection concurred with inhibition of glutamate-mediated induction of the caspase-3-related cysteine protease and coincided with marked reduction of neurons with morphological features of apoptosis, as found in vivo. Glutamic Acid 45-54 caspase 3 Mus musculus 81-90 16386699-1 2006 A probe consisting of Discosoma red fluorescent protein (DsRed) and enhanced yellow fluorescent protein (EYFP) linked by a 19-amino-acid chain containing the caspase-3 cleavage site Asp-Glu-Val-Asp was developed to monitor caspase-3 activation in living cells. Glutamic Acid 186-189 caspase 3 Mus musculus 158-167 15446579-7 2004 However, inhibition of NMDA receptors with MK-801 completely suppressed caspase 3 activation, pointing to glutamate neurotoxicity as the upstream inducer of the observed cell death. Glutamic Acid 106-115 caspase 3 Mus musculus 72-81 16023257-4 2005 The involvement of caspase-3, Bcl-2 and caspase-8 in glutamate-induced cytotoxicity was determined by immunoblots and/or real time RT-PCR. Glutamic Acid 53-62 caspase 3 Mus musculus 19-28 16023257-6 2005 Application of increasing concentrations of glutamate to RGC-5 cells caused a dose-dependent increase in the level of cell death after 24 h. There was a glutamate-stimulated increase in the expression of caspase-8 and caspase-3 and a corresponding decrease in Bcl-2. Glutamic Acid 44-53 caspase 3 Mus musculus 218-227 16023257-6 2005 Application of increasing concentrations of glutamate to RGC-5 cells caused a dose-dependent increase in the level of cell death after 24 h. There was a glutamate-stimulated increase in the expression of caspase-8 and caspase-3 and a corresponding decrease in Bcl-2. Glutamic Acid 153-162 caspase 3 Mus musculus 218-227 16023257-7 2005 The active fragment of caspase-3 increased in glutamate-treated cells. Glutamic Acid 46-55 caspase 3 Mus musculus 23-32 11597762-0 2001 Caspase-3 activation and DNA fragmentation in primary hippocampal neurons following glutamate excitotoxicity. Glutamic Acid 84-93 caspase 3 Mus musculus 0-9 11597762-8 2001 After glutamate stimulation (125 microM), the majority of neurons was dying between 12 and 24 h. The absolute number of active caspase-3 neurons increased only moderately but in relation of surviving neurons after 24 h from 8 to 36% (125 microM), to 53% (250 microM) or to 32% (500 microM). Glutamic Acid 6-15 caspase 3 Mus musculus 127-136 11597762-10 2001 In our system, glutamate-mediated excitotoxicity effects the DNA fragmentation and caspase-3 activation. Glutamic Acid 15-24 caspase 3 Mus musculus 83-92 11428862-11 2001 Immunohistochemical analysis of activated caspase-3 revealed numerous positively labelled neurons in the ganglion cell layer in homocysteine and homocysteine/glutamate-injected eyes, but not in PBS-injected eyes. Glutamic Acid 158-167 caspase 3 Mus musculus 42-51 10321830-7 1999 Our studies indicate that C5a may inhibit glutamate-mediated neuronal death through partial inhibition of caspase-3 activity. Glutamic Acid 42-51 caspase 3 Mus musculus 106-115 8987778-3 1997 We have studied the activation of the CED3/ICE-related protease CPP32 in two in vitro models of mouse cerebellar granule neuronal cell death: K+/serum deprivation-induced apoptosis and glutamate-induced necrosis. Glutamic Acid 185-194 caspase 3 Mus musculus 64-69 9570797-1 1998 We examined the expression, activation, and cellular localization of caspase-3 (CPP32) using immunohistochemistry, immunoblots, and cleavage of the fluorogenic substrate N-benzyloxycarbonyl-Asp-Glu-Val-Asp-7-amino-4-trifluoromethyl coumarin (zDEVD-afc) in adult mouse brain after temporary (2 hr) middle cerebral artery occlusion produced by filament insertion into the carotid artery. Glutamic Acid 194-197 caspase 3 Mus musculus 69-78 9570797-1 1998 We examined the expression, activation, and cellular localization of caspase-3 (CPP32) using immunohistochemistry, immunoblots, and cleavage of the fluorogenic substrate N-benzyloxycarbonyl-Asp-Glu-Val-Asp-7-amino-4-trifluoromethyl coumarin (zDEVD-afc) in adult mouse brain after temporary (2 hr) middle cerebral artery occlusion produced by filament insertion into the carotid artery. Glutamic Acid 194-197 caspase 3 Mus musculus 80-85 35338672-13 2022 Treatment with CP ameliorates the expression of Bax, Bcl-2 and caspase-3 in the brain tissue of glutamate induced brain injured mice. Glutamic Acid 96-105 caspase 3 Mus musculus 63-72