PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11025193-7 2000 During spontaneous and H2O2-induced apoptosis, the activity of caspase-3 is significantly increased. Hydrogen Peroxide 23-27 caspase 3 Mus musculus 63-72 34829088-5 2021 FST also diminished H2O2-induced activation of caspase-3, which was associated with the ability of FST to protect the degradation of poly (ADP-ribose) polymerase. Hydrogen Peroxide 20-24 caspase 3 Mus musculus 47-56 34374636-5 2021 At a concentration-dependent way, resveratrol reversed H2O2-induced increases in expressions of cleaved caspase-3 and cleaved caspase-9, production of ROS, loss of mitochondrial membrane potential and the expressions of p-p38, p-ERK, and p-JNK. Hydrogen Peroxide 55-59 caspase 3 Mus musculus 104-113 34769159-7 2021 Furthermore, AEMR diminished H2O2-induced activation of caspase-3, which was associated with the ability of AEMR to block the degradation of poly (ADP-ribose) polymerase, thereby attenuating H2O2-induced apoptosis. Hydrogen Peroxide 191-195 caspase 3 Mus musculus 56-65 34278519-6 2021 Knockdown of FENDRR augmented Nrf2 and HO-1 protein levels and testosterone production in H2O2-treated TM3 cells, whereas the apoptosis rate and caspase 3 activity were decreased. Hydrogen Peroxide 90-94 caspase 3 Mus musculus 145-154 32649980-9 2020 SAC treatment also moderated the degradation of muscle-specific proteins (MHCf) in the H2O2-treated myotubes supported by lower induction of diverse proteolytic systems (i.e. cathepsin, calpain, ubiquitin-proteasome E3-ligases, caspase-3, autophagy). Hydrogen Peroxide 87-91 caspase 3 Mus musculus 228-237 34679653-6 2021 Sesamol suppressed H2O2-induced expression of phospho-IKKalpha, p53, and caspase-3. Hydrogen Peroxide 19-23 caspase 3 Mus musculus 73-82 34542904-7 2021 ROS production, CCL2 level, cardiomyocyte apoptosis, and expression of Bax, caspase-3, and p-p38 MAPK were significantly amplified by the administration of IL-39 combined with H2O2, and these processes were significantly alleviated by an antioxidant Trolox. Hydrogen Peroxide 176-180 caspase 3 Mus musculus 76-85 35585377-4 2022 The numbers of cleaved-Caspase-3-positive cells and protein expression of Caspase-9 induced by H2O2 treatment were decreased by UC-MSC-CM treatment. Hydrogen Peroxide 95-99 caspase 3 Mus musculus 23-32 35471621-7 2022 Moreover, CFE blocked H2O2-induced cytosolic release of cytochrome c, activation of caspase-9 and caspase-3, and degradation of poly (ADP-ribose) polymerase. Hydrogen Peroxide 22-26 caspase 3 Mus musculus 98-107 34769159-7 2021 Furthermore, AEMR diminished H2O2-induced activation of caspase-3, which was associated with the ability of AEMR to block the degradation of poly (ADP-ribose) polymerase, thereby attenuating H2O2-induced apoptosis. Hydrogen Peroxide 29-33 caspase 3 Mus musculus 56-65 34449318-11 2021 Treatment of CMs with H2O2 notably induced irregular beating and decreased the amplitude of the beating signal of CMs, concomitantly with increased caspase-3/7 activity. Hydrogen Peroxide 22-26 caspase 3 Mus musculus 148-159 34542904-6 2021 IL-39 and H2O2 both significantly promoted the production of intracellular ROS, increased the level of intracellular CCL2, stimulated the apoptotic progress of cardiomyocytes, increased the mRNA and protein expression levels of Bax, caspase-3, and p-p38 MAPK, and decreased the mRNA and protein expression levels of Bcl-2. Hydrogen Peroxide 10-14 caspase 3 Mus musculus 233-242 33569454-7 2021 In the H2O2-induced 661W cell model, H2O2 increased cellular apoptosis rates, the expression levels of Bcl-2-associated X-protein (BAX) and cleaved caspase 3, reactive oxygen species (ROS) production, and malondialdehyde content, while decreasing the cell viability, and Bcl-2, superoxide dismutase, catalase, and glutathione peroxidase activity. Hydrogen Peroxide 7-11 caspase 3 Mus musculus 148-157 33569454-7 2021 In the H2O2-induced 661W cell model, H2O2 increased cellular apoptosis rates, the expression levels of Bcl-2-associated X-protein (BAX) and cleaved caspase 3, reactive oxygen species (ROS) production, and malondialdehyde content, while decreasing the cell viability, and Bcl-2, superoxide dismutase, catalase, and glutathione peroxidase activity. Hydrogen Peroxide 37-41 caspase 3 Mus musculus 148-157 32365512-5 2020 In addition, p66shc knockdown using p66shc siRNA reduced the expression levels of cleaved caspase-3, p62, and PINK1, as well as proinflammatory mediators in the H2O2-treated HT22 neuronal cells. Hydrogen Peroxide 161-165 caspase 3 Mus musculus 90-99 31746021-6 2019 Moreover, we found that miR-142 reduced the Bcl-2/Bax ratio and upregulated hydrogen peroxide (H2 O2 )-induced caspase-3 expression. Hydrogen Peroxide 76-93 caspase 3 Mus musculus 111-120 31191799-9 2019 Moreover, AMO-155 reversed the H2O2-induced downregulation of Bcl-2 and XIAP and upregulation of Bax and cleaved-caspase-3. Hydrogen Peroxide 31-35 caspase 3 Mus musculus 113-122 30601695-5 2019 Our data indicated that lunasin attenuated H2O2-induced, mitochondria-dependent endothelial apoptosis via down-regulating Bax and up-regulating Bcl-2, inhibiting the mitochondrial depolarization, and reducing the release of cytochrome c, as well as decreasing the activation of caspase-9 and caspase-3 in vitro and in vivo. Hydrogen Peroxide 43-47 caspase 3 Mus musculus 292-301 30320895-6 2019 Meanwhile, knockdown of TDP-43 attenuated the expression of the proapoptotic proteins Bax and Cytochrome c, elevated the anti-apoptotic protein Bcl-2, and suppressed the activation of caspase 3 in H2 O2 -induced RGC-5 cells. Hydrogen Peroxide 197-202 caspase 3 Mus musculus 184-193 31019651-7 2019 We also found that gamma-mangostin, not alpha-mangostin, significantly inhibited H2O2-induced DNA fragmentation and activation of caspases 3 and 9, demonstrating its antiapoptotic action. Hydrogen Peroxide 81-85 caspase 3 Mus musculus 130-146 28784051-5 2019 Effects of urolithins on apoptosis and caspase 3/7 and 9 release from H2O2-induced oxidative stress of BV-2 and SH-SY5Y cells were assessed. Hydrogen Peroxide 70-74 caspase 3 Mus musculus 39-56 28784051-9 2019 Urolithins mitigated apoptosis and caspase 3/7 and 9 release from H2O2-induced oxidative stress of BV-2 and SH-SY5Y cells. Hydrogen Peroxide 66-70 caspase 3 Mus musculus 35-52 29898376-7 2018 A2BAR activation decreased H2O2-induced cell apoptosis in vitro, as characterized by the translocation of apoptotic proteins, the release of cytochrome c, and the activation of caspase-3 and poly (ADP ribose) polymerase 1 (PARP-1). Hydrogen Peroxide 27-31 caspase 3 Mus musculus 177-221 30533172-10 2018 Coherently, apoptotic gene expressions (Casp3, Casp9, Bax, and Parp8) were significantly increased in the retina with increasing dosages of H2O2, while Bcl2 expression was mildly decreased. Hydrogen Peroxide 140-144 caspase 3 Mus musculus 40-45 30119261-8 2018 Furthermore, the blocking of H2O2-induced apoptosis by schisandrin A was associated with the inhibition of poly (ADP-ribose) polymerase degradation by the inactivation of caspase-3. Hydrogen Peroxide 29-33 caspase 3 Mus musculus 171-180 29629628-5 2018 Furthermore, PEPF not only decreased the expression of Bax, cytochrome c, and cleaved caspases-3, -8, and -9, but also increased the expression of PARP and Bcl-2 in the H2O2-treated HT22 hippocampus cells, which overall contributed to the neuroprotective action. Hydrogen Peroxide 169-173 caspase 3 Mus musculus 86-108 30116378-6 2018 Reverse transcription-polymerase chain reaction and western blot results indicated that HNK significantly decreased the expression of mRNA and cleaved protein of caspase-3 and caspase-9 in podocytes pre-treated with H2O2. Hydrogen Peroxide 216-220 caspase 3 Mus musculus 162-171 29678743-11 2018 Over-expression of GPX1 reduced the active level of Caspase3 after H2O2 treatment. Hydrogen Peroxide 67-71 caspase 3 Mus musculus 52-60 29259391-7 2017 Finally, Fas/FasL and caspase-3 mRNA was analyzed with q-PCR and immunocytochemistry in cells treated with H2O2 and/or MEL. Hydrogen Peroxide 107-111 caspase 3 Mus musculus 22-31 29697031-0 2018 TPEN Exerts Antitumor Efficacy in Murine Mammary Adenocarcinoma Through an H2O2 Signaling Mechanism Dependent on Caspase-3. Hydrogen Peroxide 75-79 caspase 3 Mus musculus 113-122 29330344-6 2018 RESULTS: We showed that both N- and C-terminal PTHrP peptides at 100 nM decreased reactive oxygen species production and forkhead box protein O activation following hydrogen peroxide (H2O2)-induced oxidation, which was related to decreased lipid oxidative damage and caspase-3 activation in these cells. Hydrogen Peroxide 165-182 caspase 3 Mus musculus 267-276 29330344-6 2018 RESULTS: We showed that both N- and C-terminal PTHrP peptides at 100 nM decreased reactive oxygen species production and forkhead box protein O activation following hydrogen peroxide (H2O2)-induced oxidation, which was related to decreased lipid oxidative damage and caspase-3 activation in these cells. Hydrogen Peroxide 184-188 caspase 3 Mus musculus 267-276 29259391-0 2017 Melatonin partially protects 661W cells from H2O2-induced death by inhibiting Fas/FasL-caspase-3. Hydrogen Peroxide 45-49 caspase 3 Mus musculus 87-96 29259391-14 2017 Fas, FasL, and caspase-3 expression was increased in cells treated with H2O2, and this effect was prevented by MEL. Hydrogen Peroxide 72-76 caspase 3 Mus musculus 15-24 29259391-15 2017 Finally, MEL treatment partially prevented the activation of caspase-3 caused by H2O2. Hydrogen Peroxide 81-85 caspase 3 Mus musculus 61-70 29259391-17 2017 MEL can prevent photoreceptor cell death induced by H2O2 via the inhibition of the proapoptotic pathway Fas/FasL-caspase-3. Hydrogen Peroxide 52-56 caspase 3 Mus musculus 113-122 28798484-5 2017 In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2. Hydrogen Peroxide 61-65 caspase 3 Mus musculus 107-116 27324899-6 2017 In addition, downregulation of TMEM59L prevented neuronal cell death and caspase-3 activation caused by hydrogen peroxide insults and reduced the lipidation of LC3B. Hydrogen Peroxide 104-121 caspase 3 Mus musculus 73-82 28784995-7 2017 Meanwhile, miR-98 overexpression attenuated the upregulation of Fas and caspase-3 in H2O2-treated cardiomyocytes at the mRNA and protein levels. Hydrogen Peroxide 85-89 caspase 3 Mus musculus 72-81 27579673-7 2017 In vitro studies demonstrated increased survival of GREM1-MSCs exposed to H2 O2 , which is consistent with the activation of caspase-3. Hydrogen Peroxide 74-79 caspase 3 Mus musculus 125-134 28342843-8 2017 Further investigation of underlying mechanisms of NR4A1"s protective effects showed that NR4A1 overexpression in MIN6 cells reduced Caspase 3 activation caused by H2O2, and increased expression of WT1 and SOD1. Hydrogen Peroxide 163-167 caspase 3 Mus musculus 132-141 27575480-4 2016 The inhibition effect of FDP-Sr on cell apoptosis induced by H2O2 was proved by reduced reactive oxygen species production and activated caspase3. Hydrogen Peroxide 61-65 caspase 3 Mus musculus 137-145 27787886-7 2017 Moreover, Ngb blocks the stimulation of Bax (pro-apoptotic) and the inhibition of Bcl-2 (anti-apoptotic) gene expression induced by H2 O2 , which in turn abolishes caspase 3 activation. Hydrogen Peroxide 132-137 caspase 3 Mus musculus 164-173 27787886-8 2017 The protective effect of Ngb upon H2 O2 induced activation of caspase 3 activity and cell death can be accounted for by activation of protein kinase A and mitogen-activated protein kinase transduction cascade. Hydrogen Peroxide 34-39 caspase 3 Mus musculus 62-71 27786251-9 2016 Gene expression analysis showed significantly reduced expressions of PRX1 and caspase-3 in the pretreatment groups when compared with cells treated with H2O2 alone. Hydrogen Peroxide 153-157 caspase 3 Mus musculus 78-87 27786251-10 2016 Also, a decrease of caspase-3 expressions was observed in PRX1 knockout MC3T3-E1 cells with or without H2O2 in comparison to wild-type cells. Hydrogen Peroxide 103-107 caspase 3 Mus musculus 20-29 27352334-9 2015 In addition, APS promoted the expression of protein Bcl-2 in H2O2-treated C2C12 cells, but did not change Bax, thus reducing the Bax/Bcl-2 ratio that in turn prevented the release of cytochrome c and the activation of caspase-3. Hydrogen Peroxide 61-65 caspase 3 Mus musculus 218-227 25550457-7 2015 In this work, we demonstrate that in pro-B-lymphoblastic cells (Ba/F3), treated with H2O2, PI-PLCbeta1b conferred resistance to cell death, promoting cell cycle progression and cell proliferation and influencing the expression of cyclin A and E. Interestingly, we found that, expression of PI-PLCbeta1b affects the activity of caspase-3, caspase-7, and of several protein kinases induced by oxidative stress. Hydrogen Peroxide 85-89 caspase 3 Mus musculus 327-336 25740141-5 2015 Furthermore, the mRNA expression of TNF-alpha and NF-kB were significantly increased in H2O2-treated C2C12 cells, while pre-treatment with Sunphenon (50 mug/mL)/Polyphenon 60 (50 mug/mL) significantly (p<0.05) down-regulated it when compared to the untreated control group.Subsequent analysis of DNA degeneration and caspase activation revealed that Sunphenon (50 mug/mL)/Polyphenon 60 (50 mug/mL) inhibited activation of caspase-3 and showed an inhibitory effect on DNA degradation. Hydrogen Peroxide 88-92 caspase 3 Mus musculus 425-434 25090966-6 2014 Furthermore, the overexpression of Sirt3 attenuated the release of cytochrome c, the increase in the Bax/Bcl-2 ratio, as well as caspase-9/caspase-3 activity induced by H(2)O(2), and eventually inhibited apoptotic neuronal cell death. Hydrogen Peroxide 169-177 caspase 3 Mus musculus 139-148 25366368-7 2015 H2O2 treatment significantly increased the fluorescence intensities of 8-OHdG and gammaH2AX, reduced the intensity of MitoTracker Red in the mitochondria, increased HEL concentrations in GCs, and enhanced the number of apoptotic cells and caspase-3/7 activities. Hydrogen Peroxide 0-4 caspase 3 Mus musculus 239-248 25280466-7 2014 In vitro study demonstrated that miR-23a-3p decreased hydrogen peroxide (H2O2)-induced lactate dehydrogenase (LDH) leakage dose-dependently, and reduced protein levels of activated caspase-3 in neuro-2a cells. Hydrogen Peroxide 54-71 caspase 3 Mus musculus 181-190 25280466-7 2014 In vitro study demonstrated that miR-23a-3p decreased hydrogen peroxide (H2O2)-induced lactate dehydrogenase (LDH) leakage dose-dependently, and reduced protein levels of activated caspase-3 in neuro-2a cells. Hydrogen Peroxide 73-77 caspase 3 Mus musculus 181-190 25435295-6 2015 Our results revealed that H2O2 increased the rate of apoptosis by stimulating various pro-apoptotic processes, such as the generation of intracellular reactive oxygen species (ROS), lipid peroxidation, DNA fragmentation and caspase-3 activation. Hydrogen Peroxide 26-30 caspase 3 Mus musculus 224-233 24252591-5 2014 Purified Tat-GLO protein efficiently transduced into HT-22 neuronal cells and protected cells against MG- and H2O2-induced cell death, DNA fragmentation, and activation of caspase-3 and mitogen-activated protein kinase. Hydrogen Peroxide 110-114 caspase 3 Mus musculus 172-181 24825375-5 2014 H2O2-induced apoptosis in C2C12 cells were determined by mRNA expression of caspase-3. Hydrogen Peroxide 0-4 caspase 3 Mus musculus 76-85 24825375-8 2014 Pretreatment with MPG or T.peptides is also found to significantly (p < 0.05) decrease the mRNA expression of caspase-3 in H2O2-induced C2C12 cells. Hydrogen Peroxide 126-130 caspase 3 Mus musculus 113-122 24835026-6 2014 Further, the H2O2 induced cell death was arrested in the presence of CWC through the inhibition of CDC42 mediated SAPK/JNK pathways and activation of other molecules of apoptotic pathways, including Bax and caspase3. Hydrogen Peroxide 13-17 caspase 3 Mus musculus 207-215 21654327-2 2011 In cultured endothelial cells, 2 atherogenic stimuli, hydrogen peroxide and tumor necrosis factor-alpha, increased the acetylation of p53 lysine-382, and caspase-3 cleavage, an indicator of apoptotic signaling. Hydrogen Peroxide 54-71 caspase 3 Mus musculus 154-163 24849190-4 2014 Western blot analysis was also used to measure the expression level of Bcl-2, Bax, caspase 9, and caspase 3 proteins in H2O2-treated RGC-5 cells. Hydrogen Peroxide 120-124 caspase 3 Mus musculus 98-107 24008831-5 2013 Exposure to H2O2 and STS enhanced ROS in mutant cells and largely increased XO activity; STS further boosted the generation of mitochondrial ROS and caspase-3 activity. Hydrogen Peroxide 12-16 caspase 3 Mus musculus 149-158 22775755-5 2012 Generation of excess intracellular ROS, nuclear localization of Bax and caspase 3 activation along with decrease of cellular viability, confirmed apoptosis induction in RGC-5 by 72 h serum starvation and 500 M H2O2 exposure for 1 h. Nuclear swelling as supported by nuclear cytoplasmic ratio and conspicuous black spots with nuclear remodelling were observed only upon SFM, but not with H2O2 treatment. Hydrogen Peroxide 210-214 caspase 3 Mus musculus 72-81 22138401-4 2012 Quercetin suppressed H(2)O(2)-induced apoptotic events, including hypodiploid cells, activation of caspase 3 enzyme activity and lactate dehydrogenase release. Hydrogen Peroxide 21-29 caspase 3 Mus musculus 99-108 22003875-6 2011 In addition, 70 muM hispidin significantly scavenged intracellular ROS and inhibited apoptosis and caspase-3 induced by hydrogen peroxide. Hydrogen Peroxide 120-137 caspase 3 Mus musculus 99-108 23742763-5 2013 H2O2 caused a concentration-dependent reduction in cell viability associated with caspase 3 activation. Hydrogen Peroxide 0-4 caspase 3 Mus musculus 82-91 21091646-7 2011 KEY RESULTS: NaHS suppressed DNA fragmentation and the activities of caspase-3 and -7 induced by palmitate, the cytokines or hydrogen peroxide. Hydrogen Peroxide 125-142 caspase 3 Mus musculus 69-85 21273783-6 2011 VSMC apoptosis in response to hydrogen peroxide was assessed by JC-1 staining, caspase-3 cleavage, annexin V, and Hoechst staining. Hydrogen Peroxide 30-47 caspase 3 Mus musculus 79-88 21266813-8 2011 We also demonstrated Hoechst staining of YAMC cells and that H2O2-induced apoptosis is significantly reduced by FGF19 treatment via inhibition of the caspase-3 pathway. Hydrogen Peroxide 61-65 caspase 3 Mus musculus 150-159 20212261-9 2010 The downstream molecule of Akt, phosphor-GSK-3beta (inactivation), was also higher, whereas caspase 3 activity was lower in females in response to hydrogen peroxide. Hydrogen Peroxide 147-164 caspase 3 Mus musculus 92-101 18336470-6 2008 At low dosages, TGF-beta1 enhanced (by approximately 76%) cell survival against hydrogen peroxide treatment via inactivation of caspase-3 and -9. Hydrogen Peroxide 80-97 caspase 3 Mus musculus 128-144 19998489-3 2010 In wild-type neurons, PDGF-BB enhanced the survival of these neurons and suppressed H(2)O(2)-induced caspase-3 activation. Hydrogen Peroxide 84-92 caspase 3 Mus musculus 101-110 19557877-7 2009 Hydrogen peroxide treatment also induced phosphorylation of the mitogen-activated protein kinases (MAPKs), c-Jun terminal kinase (JNK), extracellular-regulated kinase (ERK) and p38, and activated caspase-3. Hydrogen Peroxide 0-17 caspase 3 Mus musculus 196-205 19557877-8 2009 Pretreatment with erigeroflavanone inhibited hydrogen peroxide-induced activation of MAPKs and caspase-3. Hydrogen Peroxide 45-62 caspase 3 Mus musculus 95-104 18330893-14 2008 DHT inhibited the H2O2-induced increase in caspase-3 expression and decreased the level of Bcl-2 and the cellular inhibitor of apoptosis protein (cIAP)-2. Hydrogen Peroxide 18-22 caspase 3 Mus musculus 43-52 20164595-4 2010 Here, we observed that the cells bearing high level of Abeta were more vulnerable than the controls to H2O2-induced apoptosis, and this effect of Abeta was associated with decrease of Bcl-2, elevation of Bax and cytosolic cytochrome-c, as well as activation of caspase-3, suggesting that Abeta could potentiate the oxidant-induced cell apoptosis with involvement of mitochondria-caspase-3 pathway. Hydrogen Peroxide 103-107 caspase 3 Mus musculus 261-270 20164595-4 2010 Here, we observed that the cells bearing high level of Abeta were more vulnerable than the controls to H2O2-induced apoptosis, and this effect of Abeta was associated with decrease of Bcl-2, elevation of Bax and cytosolic cytochrome-c, as well as activation of caspase-3, suggesting that Abeta could potentiate the oxidant-induced cell apoptosis with involvement of mitochondria-caspase-3 pathway. Hydrogen Peroxide 103-107 caspase 3 Mus musculus 379-388 18518937-11 2008 Furthermore, Cot/Tpl2-deficient TECs demonstrated significantly less caspase-3 activation after hydrogen peroxide stimulation with comparable caspase-9 activation to wild type TEC. Hydrogen Peroxide 96-113 caspase 3 Mus musculus 69-78 17438522-3 2007 H(2)O(2)-induced changes in caspase-3 activity and mitochondrial permeability transition (MPT) were determined. Hydrogen Peroxide 0-8 caspase 3 Mus musculus 28-37 17532486-5 2007 H(2)O(2)-induced apoptotic events including hypodiploid cells, DNA fragmentation, activation of caspase 3 enzyme activity, and a loss in the mitochondrial membrane potential with the concomitant release of cytochrome c from mitochondria to the cytosol were suppressed by the addition of BE but not BI. Hydrogen Peroxide 0-8 caspase 3 Mus musculus 96-105 16585560-2 2006 H2O2-treated cells showed apoptotic features, such as activation of caspase-9 and caspase-3, nuclear fragmentation, and DNA fragmentation. Hydrogen Peroxide 0-4 caspase 3 Mus musculus 82-91 17204664-6 2007 In vitro, H2O2 stimulation significantly induced apoptosis of VSMCs as evidenced by the 3- and 3.2-fold increases of cleaved caspase-3 compared with those in the control group by Western blot and flow cytometric analyses, respectively (P<0.01). Hydrogen Peroxide 10-14 caspase 3 Mus musculus 125-134 17204664-8 2007 Administration of SCF (10 to 1000 ng/mL) significantly lowered the amount of cleaved caspase-3 in H2O2-treated VSMCs (P<0.01). Hydrogen Peroxide 98-102 caspase 3 Mus musculus 85-94 16934799-7 2006 Moreover, H(2)O(2)-induced apoptotic signals, such as c-JUN N-terminal kinase activation, cytochrome c release, caspase 3 activation, and poly (ADP-ribose) polymerase cleavage were all down-regulated by the intracellular Ca(2+) chelation. Hydrogen Peroxide 10-18 caspase 3 Mus musculus 112-121 16616712-7 2006 Contributions from both apoptotic and necrotic pathways were implicated in the H2O2-induced cell loss as was demonstrated by the use of the caspase-3 inhibitor (Z-DEVD-fmk) and the PARP-1 inhibitor (DPQ). Hydrogen Peroxide 79-83 caspase 3 Mus musculus 140-149 15871184-7 2005 RESULTS: H2O2 ( 0.5 mmol/L ) activated caspase-3, caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2-induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells. Hydrogen Peroxide 9-13 caspase 3 Mus musculus 39-48 15965073-7 2005 p38 mitogen-activated protein kinase (MAPK) and caspase-3 were also activated in BV-2 cells under H2O2 stress. Hydrogen Peroxide 98-102 caspase 3 Mus musculus 48-57 15965073-8 2005 Sesamolin was able to inhibit H2O2-induced p38 MAPK and caspase-3 activation and cell death. Hydrogen Peroxide 30-34 caspase 3 Mus musculus 56-65 16220659-11 2005 The stimulation of 5-HT1A receptor by 5-CT produced a dramatic protection against H2O2-triggered activation of caspase-3 and reduction in levels of MAG-IR. Hydrogen Peroxide 82-86 caspase 3 Mus musculus 111-120 16220659-10 2005 Treatment with H2O2 caused the activation of caspase-3-positive cells and the reduction in levels of MAG-IR in the limbic neuron/glia cocultures as compared to medium alone. Hydrogen Peroxide 15-19 caspase 3 Mus musculus 45-54 15871184-7 2005 RESULTS: H2O2 ( 0.5 mmol/L ) activated caspase-3, caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2-induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells. Hydrogen Peroxide 9-13 caspase 3 Mus musculus 235-244 15165989-11 2004 Thus H(2)O(2)-induced cell death in OPN-deficient cardiac fibroblasts is mediated by a caspase-3-independent, necrotic pathway. Hydrogen Peroxide 5-13 caspase 3 Mus musculus 87-96 14631147-7 2003 Activation of caspase 3 by H2O2 was more pronounced in LD than in MD and HD. Hydrogen Peroxide 27-31 caspase 3 Mus musculus 14-23 16136992-7 2004 Heat shock response could inhibit the release of cytochrome c from mitochondria to cytoplasm,the activation of caspase -3,8,9 and the subsequent apoptosis induced by H2O2 in C2C12 cell. Hydrogen Peroxide 166-170 caspase 3 Mus musculus 111-125 14556862-8 2003 Interestingly, hydrogen peroxide-induced oxidative apoptosis of MLE-12 cells, with a shrinking nuclear morphology and activated caspase-3 activity, is also mediated by AP-1, JNK, and p38. Hydrogen Peroxide 15-32 caspase 3 Mus musculus 128-137 11931670-4 2002 After treatment with H(2)O(2), PKC-dependent phosphorylation of Bcl-2 and cell viability of Plcg1(-/-) cells decreased dramatically and caspase-3-like activity increased significantly compared with that of the wild-type cells. Hydrogen Peroxide 21-29 caspase 3 Mus musculus 136-145 12180991-5 2002 Over-expression of Hsp105alpha enhanced hydrogen peroxide-induced apoptosis by enhancing the activation of caspase-3, poly(ADP-ribose)polymerase cleavage, cytochrome c release and activation of p38 mitogen-activated protein kinase (p38). Hydrogen Peroxide 40-57 caspase 3 Mus musculus 107-116