PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18840762-3 2008 Moreover, inhibitors of caspase-3 and -8 completely attenuated both ROS formation and total protein degradation induced by TNF-alpha/IFN-gamma and ANG II. Reactive Oxygen Species 68-71 caspase 3 Mus musculus 24-40 19404720-3 2009 Specific inhibitors of caspase-3/-8 completely attenuated ROS production, total protein degradation and the LPS-induced autophosphorylation of dsRNA-dependent protein kinase (PKR). Reactive Oxygen Species 58-61 caspase 3 Mus musculus 23-35 18973755-8 2009 These results suggest that high glucose induces muscle atrophy through the caspase-3/-8 induced activation of PKR, leading to phosphorylation of eIF2alpha and depression of protein synthesis, together with PKR-mediated ROS production, through p38MAPK and increased protein degradation. Reactive Oxygen Species 219-222 caspase 3 Mus musculus 75-87 19016762-5 2008 MB-PDT could induce intense apoptotic cell death through a series of steps beginning with the photochemical generation of reactive oxygen species that activate the caspase-9/caspase-3 apoptosis pathway. Reactive Oxygen Species 122-145 caspase 3 Mus musculus 174-183 18762247-3 2008 We show for the first time that curcumin-induced rapid ROS generation causes the release of apoptosis inducing factor (AIF) from the mitochondria to the cytosol and nucleus, hence, leading to caspase 3-independent apoptosis. Reactive Oxygen Species 55-58 caspase 3 Mus musculus 192-201 19706975-5 2008 This combination markedly induced intracellular levels of reactive oxygen species (ROS) starting at 6 h and significantly decreased the mitochondrial potential starting at 12 h. The combination significantly elevated caspase-9 and caspase-3 activities at 24 and 48 h. The combination also induced hypomethylation (at 24 and 48 h), as indicated by significantly decreased 5-methyldeoxycytidine levels and SAM/SAH ratios. Reactive Oxygen Species 83-86 caspase 3 Mus musculus 231-240 18049903-10 2008 In conclusion, ACh prevented the hypoxia-induced apoptosis of mouse ES cells by inhibiting the ROS-mediated p38 MAPK and JNK activation as well as the regulation of Bcl-2, c-IAPs, and caspase-3. Reactive Oxygen Species 95-98 caspase 3 Mus musculus 184-193 11488598-4 2001 Pretreatment of cells with N-acetylcysteine, a scavenger of reactive oxygen species (ROS), conferred resistance to the induction of the membrane depolarization, cytochrome c release, and caspase-3 activation by SA-liposomes. Reactive Oxygen Species 60-83 caspase 3 Mus musculus 187-196 16728380-10 2006 Inhibition of caspase-3 protected oxidative stress produced by cadmium, suggesting that the activation of caspase-3 also contributes to generation of reactive oxygen species (ROS). Reactive Oxygen Species 150-173 caspase 3 Mus musculus 14-23 16728380-10 2006 Inhibition of caspase-3 protected oxidative stress produced by cadmium, suggesting that the activation of caspase-3 also contributes to generation of reactive oxygen species (ROS). Reactive Oxygen Species 150-173 caspase 3 Mus musculus 106-115 16728380-10 2006 Inhibition of caspase-3 protected oxidative stress produced by cadmium, suggesting that the activation of caspase-3 also contributes to generation of reactive oxygen species (ROS). Reactive Oxygen Species 175-178 caspase 3 Mus musculus 14-23 16728380-10 2006 Inhibition of caspase-3 protected oxidative stress produced by cadmium, suggesting that the activation of caspase-3 also contributes to generation of reactive oxygen species (ROS). Reactive Oxygen Species 175-178 caspase 3 Mus musculus 106-115 15050407-3 2004 Mercury-induced intracellular calcium modulated reactive oxygen species (ROS) production, which resulted in both cell apoptosis and necrosis indicated by annexin V binding and caspase-3 activity, and propidium-iodide binding. Reactive Oxygen Species 48-71 caspase 3 Mus musculus 176-185 15050407-3 2004 Mercury-induced intracellular calcium modulated reactive oxygen species (ROS) production, which resulted in both cell apoptosis and necrosis indicated by annexin V binding and caspase-3 activity, and propidium-iodide binding. Reactive Oxygen Species 73-76 caspase 3 Mus musculus 176-185 12685655-3 2003 In this study, we report on the relationship between the UVB-induced anti-apoptotic effect and caspase-3/7 inhibition by reactive oxygen species (ROS). Reactive Oxygen Species 121-144 caspase 3 Mus musculus 95-104 12685655-3 2003 In this study, we report on the relationship between the UVB-induced anti-apoptotic effect and caspase-3/7 inhibition by reactive oxygen species (ROS). Reactive Oxygen Species 146-149 caspase 3 Mus musculus 95-104 12685655-7 2003 The prevention of proteolysis was also confirmed by both the following results: one is the inhibition of in vitro caspase-3/7 and -9 activation in cell lysates exposed to UVB in the presence of cytochrome c and dATP, which was caused by the production of ROS, and the other is the inhibition of in vitro caspase-3/7 activation in the presence of active caspase-9. Reactive Oxygen Species 255-258 caspase 3 Mus musculus 114-132 12685655-7 2003 The prevention of proteolysis was also confirmed by both the following results: one is the inhibition of in vitro caspase-3/7 and -9 activation in cell lysates exposed to UVB in the presence of cytochrome c and dATP, which was caused by the production of ROS, and the other is the inhibition of in vitro caspase-3/7 activation in the presence of active caspase-9. Reactive Oxygen Species 255-258 caspase 3 Mus musculus 114-123 12685655-8 2003 These results showed that the inhibition of the caspase cascade downstream mitochondria by ROS production, leading to a significant inhibition of caspase-3/7 activation, was one of the causes of the antiapoptotic effect by small doses of UVB irradiation. Reactive Oxygen Species 91-94 caspase 3 Mus musculus 146-155 17947235-12 2007 Moreover AVD, K+ conductances, and caspase-3 were strongly impaired by ROS scavenger N-acetylcysteine. Reactive Oxygen Species 71-74 caspase 3 Mus musculus 35-44 16380497-6 2006 Increased extracellular glucose (30 mmol/l) rapidly stimulated generation of intracellular reactive oxygen species (ROS) through NADPH oxidase and mitochondrial pathways and led to activation of proapoptotic p38 mitogen-activated protein kinase and caspase 3 and to apoptosis of conditionally immortalized podocytes in vitro. Reactive Oxygen Species 116-119 caspase 3 Mus musculus 249-258 15854745-4 2005 Several previous studies have demonstrated the involvement of ROS in Abeta-induced neurotoxicity, and ROS generated by Abeta have been reported to lead to the activation of nuclear factor-kappa B (NF-kappaB), a transcription factor; pre-treatment with melatonin in the present study reduced the level of Abeta-induced intracellular ROS generation, inhibited NF-kappaB activation, and suppressed the Abeta-induced increase in caspase-3 enzyme activity. Reactive Oxygen Species 102-105 caspase 3 Mus musculus 425-434 15854745-4 2005 Several previous studies have demonstrated the involvement of ROS in Abeta-induced neurotoxicity, and ROS generated by Abeta have been reported to lead to the activation of nuclear factor-kappa B (NF-kappaB), a transcription factor; pre-treatment with melatonin in the present study reduced the level of Abeta-induced intracellular ROS generation, inhibited NF-kappaB activation, and suppressed the Abeta-induced increase in caspase-3 enzyme activity. Reactive Oxygen Species 102-105 caspase 3 Mus musculus 425-434 12031984-16 2002 Hyperglycemia-induced myocardial apoptosis is mediated, at least in part, by activation of the cytochrome c-activated caspase-3 pathway, which may be triggered by ROS derived from high levels of glucose. Reactive Oxygen Species 163-166 caspase 3 Mus musculus 118-127 11488598-4 2001 Pretreatment of cells with N-acetylcysteine, a scavenger of reactive oxygen species (ROS), conferred resistance to the induction of the membrane depolarization, cytochrome c release, and caspase-3 activation by SA-liposomes. Reactive Oxygen Species 85-88 caspase 3 Mus musculus 187-196 11454906-10 2001 To elucidate the role of reactive oxygen species (ROS) in the activation of the cytochrome c-mediated caspase-3 activation pathway, the intracellular levels of ROS and their localization were detected by fluorescent confocal microscopy. Reactive Oxygen Species 25-48 caspase 3 Mus musculus 102-111 11454906-10 2001 To elucidate the role of reactive oxygen species (ROS) in the activation of the cytochrome c-mediated caspase-3 activation pathway, the intracellular levels of ROS and their localization were detected by fluorescent confocal microscopy. Reactive Oxygen Species 50-53 caspase 3 Mus musculus 102-111 35450406-8 2022 17-DA significantly promoted cell proliferation and alleviated apoptosis by inhibiting the generation of intracellular reactive oxygen species (ROS) to downregulate cleaved caspase-3, matrix metallopeptidase- (MMP-) 2, MMP-9, and P-P65 in bEnd.3 cells after the injury. Reactive Oxygen Species 119-142 caspase 3 Mus musculus 173-182 10463952-12 1999 Taken together, these findings suggest that mitochondrial-mediated ROS generation is a key event by which inhibition of respiration causes cell death, and identifies CPP-32 and the PARP-linked pathway as targets of mitochondrial-derived ROS-induced cell death. Reactive Oxygen Species 237-240 caspase 3 Mus musculus 166-172 35218765-8 2022 KEY FINDINGS: Our data revealed that gastric ulceration due to forced swim stress is responsible for overproduction of ROS, which may be a prime reason for mitochondrial dysfunction and induction of apoptosis via activation of Caspase-3. Reactive Oxygen Species 119-122 caspase 3 Mus musculus 227-236 35624895-12 2022 These results demonstrate that the susceptibility of OPCs and mOLs to ultrafine DEPs is, at least in part, caused by excessive ROS produced by NOX2 and the sequential changes in the expression of p53, Bax, Bcl-2, and cleaved caspase-3. Reactive Oxygen Species 127-130 caspase 3 Mus musculus 225-234 35485954-6 2022 We discovered that LS-HB located in the mitochondria of B16F10 cells was able to generate excess reactive oxygen species, which subsequently resulted in mitochondrial membrane potential loss and induced apoptosis via caspase-9 and caspase-3 pathways. Reactive Oxygen Species 97-120 caspase 3 Mus musculus 231-240 35450406-8 2022 17-DA significantly promoted cell proliferation and alleviated apoptosis by inhibiting the generation of intracellular reactive oxygen species (ROS) to downregulate cleaved caspase-3, matrix metallopeptidase- (MMP-) 2, MMP-9, and P-P65 in bEnd.3 cells after the injury. Reactive Oxygen Species 144-147 caspase 3 Mus musculus 173-182 32337854-5 2020 Ag, CuO, and ZnO induced caspase 3 generated apoptosis in both cell types is accompanied by ion shedding and generation of mitochondrial reactive oxygen species (ROS) in both cell types. Reactive Oxygen Species 137-160 caspase 3 Mus musculus 25-34 34984798-8 2022 In the vitro study, ROS as an upstream signal phosphorylated IkappaBalpha and NF-kappaB, up-regulated the NLRP3 inflammasome, increased caspase3, 6, 7, and 9 to exaggerate inflammation response, finally inducing pyroptosis in renal cells. Reactive Oxygen Species 20-23 caspase 3 Mus musculus 136-144 35080339-0 2022 PP1A prevents ROS-induced pyroptosis by inhibiting MAPK/Caspase-3 in mouse adipose tissue. Reactive Oxygen Species 14-17 caspase 3 Mus musculus 56-65 35080339-7 2022 Our results demonstrated that PP1A suppressed pyroptosis in adipocytes by inhibiting the ROS/MAPK/Caspase-3 signaling pathway and promoting M2 macrophage polarization. Reactive Oxygen Species 89-92 caspase 3 Mus musculus 98-107 33921050-11 2021 In addition, we also observed a significant fold reduction (p < 0.05) in ROS fluorescent intensity and the expression of Bax (p < 0.0001), cytochrome C (p < 0.0001), cleaved caspase-9 (p > 0.010) and cleaved caspase-3 (p < 0.0001). Reactive Oxygen Species 73-76 caspase 3 Mus musculus 208-217 33401054-6 2021 Scavenging of ROS in the presence of N-acetylcysteine (NAC) almost blocks the loss of mitochondrial membrane Deltapsim, activation of JNK, cleavage of caspase-3, -9, and an induction of apoptosis in SHK treated PEL cells. Reactive Oxygen Species 14-17 caspase 3 Mus musculus 151-164 33298902-6 2020 Concurrently, ROS mediate a decrease in the levels and activation of executioner caspases-3, -6, and -7. Reactive Oxygen Species 14-17 caspase 3 Mus musculus 81-103 33044639-19 2021 The main mechanism in the cell death and inflammatory effects of IFNgamma is mediated by stimulation of ROS-mediated caspase (caspase -3 and - 9) activations and cytokine production (TNF-alpha, IL-1beta, and IL-6) via TRPM2 activation, respectively. Reactive Oxygen Species 104-107 caspase 3 Mus musculus 126-144 32905254-11 2020 Collectively, these findings establish the dose-dependent beneficial versus deleterious effects of berberine and suggest that the mechanism underlying the deleterious effects of berberine involves a caspase-3-dependent apoptotic process acting downstream of an increase in intracellular ROS levels. Reactive Oxygen Species 287-290 caspase 3 Mus musculus 199-208 32587830-7 2020 Mechanistically, VC caused a significant increase in the levels of reactive oxygen species (ROS), which led to induced genotoxic (DNA damage) and metabolic (ATP depletion) stresses, inhibited Bcl-2 expression, and promoted Bax expression and caspase-3 cleavage. Reactive Oxygen Species 67-90 caspase 3 Mus musculus 242-251 32587830-7 2020 Mechanistically, VC caused a significant increase in the levels of reactive oxygen species (ROS), which led to induced genotoxic (DNA damage) and metabolic (ATP depletion) stresses, inhibited Bcl-2 expression, and promoted Bax expression and caspase-3 cleavage. Reactive Oxygen Species 92-95 caspase 3 Mus musculus 242-251 32337854-5 2020 Ag, CuO, and ZnO induced caspase 3 generated apoptosis in both cell types is accompanied by ion shedding and generation of mitochondrial reactive oxygen species (ROS) in both cell types. Reactive Oxygen Species 162-165 caspase 3 Mus musculus 25-34 29964317-9 2018 Our collective results imply that cell apoptosis in mouse blastocysts derived from the AgNP-pretreated oocytes via intracellular ROS generation, which is further mediated through p53-, p21-, and caspase-3-dependent regulatory mechanisms. Reactive Oxygen Species 129-132 caspase 3 Mus musculus 195-204 30660690-6 2019 The increased ROS production up-regulated the expression of p53 and Bax, and down-regulated Bcl-2 expression, which led to the activation of caspase-3, ultimately initiated cell apoptosis. Reactive Oxygen Species 14-17 caspase 3 Mus musculus 141-150 30660690-11 2019 The primary mechanism of SDT is due to the increased ROS activated the p53/Caspase 3 axis of apoptosis. Reactive Oxygen Species 53-56 caspase 3 Mus musculus 75-84 31326607-3 2019 ROS-mediated apoptosis was accompanied by the induction of the endoplasmic reticulum (ER) stress-mediated apoptotic pathway, involving CHOP/GADD153 upregulation, JNK and p38 MAPK activation, and caspase-12 and caspase-8 activation, and subsequent induction of the mitochondrial apoptotic pathway through BAK and BAX activation, mitochondrial membrane potential (Deltapsim) loss, caspase-9 and caspase-3 activation, PARP cleavage, and nucleosomal DNA fragmentation. Reactive Oxygen Species 0-3 caspase 3 Mus musculus 393-402 30361692-8 2018 Indeed, OEO/thymol increased the Reactive Oxygen Species (ROS) level leading to mitochondrial membrane potential (MMP, DeltaPsim) loss, caspase-3 activation and DNA damage caused S-phase cell cycle arrest. Reactive Oxygen Species 58-61 caspase 3 Mus musculus 136-145 29098899-10 2017 Therefore, this article first uncovers the modulatory effect of FA on radiation-induced ROS/NF-kappaB/Nrf2/p53-caspase 3-PARP axis in the duodenum and establishing biological function of FA in protecting duodenum from radiation damage with a detailed mechanistic approach. Reactive Oxygen Species 88-91 caspase 3 Mus musculus 111-120 29655793-9 2018 Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways. Reactive Oxygen Species 35-38 caspase 3 Mus musculus 289-298 29263441-6 2018 Mechanistically, we reveal that pathologic levels of TNFalpha and IL-6 inhibit erythroid colony formation and differentially affect terminal erythropoiesis through reactive oxygen species-induced caspase-3 activation and apoptosis. Reactive Oxygen Species 164-187 caspase 3 Mus musculus 196-205 28477054-7 2018 Similarly, SP notably suppressed the ROS-mediated phosphorylation of MAPK (pERK1/2, pJNK, and pp38) cascades and activation of apoptotic factor caspase-3 signaling pathway that overall contributed to the neuroprotection. Reactive Oxygen Species 37-40 caspase 3 Mus musculus 144-153 29250157-6 2018 The activity of tumor necrosis factor alpha, interleukin-6, TGF-beta1, malondialdehyde, superoxide dismutase and ROS were effectively inhibited, and the protein expression of caspase-3 and Bax were clearly suppressed by treatment with myrtol in a mouse model of PTKO. Reactive Oxygen Species 113-116 caspase 3 Mus musculus 175-184 29844673-11 2018 In K7M2 cells, ROS was easily stimulated and the apoptosis pathway was subsequently activated, accompanied by elevated expression of proapoptosis proteins (such as caspase-3) and decreased expression levels of antiapoptosis proteins (such as Bcl-2). Reactive Oxygen Species 15-18 caspase 3 Mus musculus 164-173 29079564-8 2017 Targeting mitochondrial reactive oxygen species with MitoTEMPO attenuated features of atherosclerotic plaque vulnerability in middle-aged Apoe-/-/Sod2+/- mice by lowering expression of calpain-2, caspase-3, and matrix metalloproteinase-2 and decreasing smooth muscle cell apoptosis and matrix degradation. Reactive Oxygen Species 24-47 caspase 3 Mus musculus 196-205 28086830-5 2017 However, both cytotoxicity and caspase-3 activation involved generation of Reactive Oxygen Species (ROS), which could be partially reverted by the lipid antioxidant alpha-tocopherol, but not by the hydrophilic N-acetylcysteine (NAC) indicating crucial differences in the intracellular sites exposed to oxidative stress induced by sigma-2 receptor ligands. Reactive Oxygen Species 75-98 caspase 3 Mus musculus 31-40 28491037-6 2017 In fact, the retinoid induced the activation of the apoptotic cascade related to the generation of ROS through endoplasmic reticulum stress response and upregulation of phospho c-Jun N-terminal kinases and PLAcental Bone morphogenetic protein, leading to cell death through caspase-3 cleavage. Reactive Oxygen Species 99-102 caspase 3 Mus musculus 274-283 27825878-6 2017 By virtue of confocal fluorescence imaging, the artemisinin location in lysosome, ROS-triggered LMP and ultimate cell apoptosis can be visualized with the cathepsin B and caspase-3 activatable nanoprobe. Reactive Oxygen Species 82-85 caspase 3 Mus musculus 171-180 28086830-5 2017 However, both cytotoxicity and caspase-3 activation involved generation of Reactive Oxygen Species (ROS), which could be partially reverted by the lipid antioxidant alpha-tocopherol, but not by the hydrophilic N-acetylcysteine (NAC) indicating crucial differences in the intracellular sites exposed to oxidative stress induced by sigma-2 receptor ligands. Reactive Oxygen Species 100-103 caspase 3 Mus musculus 31-40 28116245-7 2017 In conclusion, we demonstrated that 7KCHO induced apoptosis of MC3T3-E1 cells associated with ROS generation, ER stress, and caspase-3/7 activity, and the effects of 7KCHO were abolished by the ROS inhibitor NAC. Reactive Oxygen Species 194-197 caspase 3 Mus musculus 125-134 27470354-11 2016 Also, acceleration of ROS led to the phospharylation of (c-Jun N-terminal kinase (JNK) and its-related signals, as well as activation of Endoplasmic Reticulum (ER) stress, promoting the progression of apoptosis via stimulating Caspase3 expression. Reactive Oxygen Species 22-25 caspase 3 Mus musculus 227-235 27147508-6 2017 There were increased caspase -3, -8 and -9 activities when fibroblasts were treated with 0.4, 0.8 and 1.6 muM CdCl2 for 24 h. Higher intracellular calcium (Ca2+) and reactive oxygen species (ROS) levels, and enhanced efflux of extracellular Ca2+ and potassium (K+). Reactive Oxygen Species 166-189 caspase 3 Mus musculus 21-42 27147508-6 2017 There were increased caspase -3, -8 and -9 activities when fibroblasts were treated with 0.4, 0.8 and 1.6 muM CdCl2 for 24 h. Higher intracellular calcium (Ca2+) and reactive oxygen species (ROS) levels, and enhanced efflux of extracellular Ca2+ and potassium (K+). Reactive Oxygen Species 191-194 caspase 3 Mus musculus 21-42 27919735-7 2017 Also, in vitro experiments, quercetin displayed inhibitory role in LPS-induced ROS production, inflammatory response and apoptosis, which were linked with PI3K/AKT-regulated Caspase-3 and NF-kappaB activation. Reactive Oxygen Species 79-82 caspase 3 Mus musculus 174-183 27177453-8 2016 Moreover, the increase of activated caspase-3 and PARP was blocked by the ROS inhibitor antioxidant N-acetyl cysteine (NAC). Reactive Oxygen Species 74-77 caspase 3 Mus musculus 36-45 25913086-7 2015 The production of excessive ROS was NADPH oxidase-dependent, which contributed to mitochondrial structural damage and mitochondrial dysfunction in placentas, followed by the cleavage of caspase-9 and caspase-3, and finally resulted in apoptosis of trophoblasts. Reactive Oxygen Species 28-31 caspase 3 Mus musculus 200-209 29124200-3 2015 We previously demonstrated that deletion of Bax or caspase 3 from these cells reduces ROS/RS production to near baseline levels indicating a central role for both Bax and caspase 3 in generating the ROS/RS. Reactive Oxygen Species 86-89 caspase 3 Mus musculus 51-60 29124200-3 2015 We previously demonstrated that deletion of Bax or caspase 3 from these cells reduces ROS/RS production to near baseline levels indicating a central role for both Bax and caspase 3 in generating the ROS/RS. Reactive Oxygen Species 86-89 caspase 3 Mus musculus 171-180 29124200-3 2015 We previously demonstrated that deletion of Bax or caspase 3 from these cells reduces ROS/RS production to near baseline levels indicating a central role for both Bax and caspase 3 in generating the ROS/RS. Reactive Oxygen Species 199-202 caspase 3 Mus musculus 51-60 29124200-3 2015 We previously demonstrated that deletion of Bax or caspase 3 from these cells reduces ROS/RS production to near baseline levels indicating a central role for both Bax and caspase 3 in generating the ROS/RS. Reactive Oxygen Species 199-202 caspase 3 Mus musculus 171-180 29124200-7 2015 These and our previous findings indicate that Bax and caspase 3 are necessary for the increased ROS/RS after withdrawing NGF from these cells and that little or none of the increased ROS/RS are secondary to a depletion of cytochrome c from the electron transport chain. Reactive Oxygen Species 96-99 caspase 3 Mus musculus 54-63 22223438-7 2014 Therefore, a possible signaling pathway in TBT-induced apoptosis in mouse livers involves PP2A inhibition and ROS elevation serving a pivotal function as upstream activators of MAPKs; activation of MAPKs in turn leads to an increase in the Bax/Bcl-2 ratio, ultimately leading to the activation of caspase-3. Reactive Oxygen Species 110-113 caspase 3 Mus musculus 297-306 25692960-5 2015 The UCNPs@TiO2 NCs endocytosed by cancer cells are able to generate intracellular ROS under NIR irradiation, decreasing the mitochondrial membrane potential to release cytochrome c into the cytosol and then activating caspase 3 to induce cancer cell apoptosis. Reactive Oxygen Species 82-85 caspase 3 Mus musculus 218-227 25456994-9 2014 The amount of reactive oxygen species (ROS) in C2C12 cells analysed with Au-NPs (in a dose-dependent manner), and the RT-PCR data demonstrated the up-regulation of caspase-3 and caspase-7 genes in C2C12 cells after treatment with Au-NPs. Reactive Oxygen Species 14-37 caspase 3 Mus musculus 164-173 25456994-9 2014 The amount of reactive oxygen species (ROS) in C2C12 cells analysed with Au-NPs (in a dose-dependent manner), and the RT-PCR data demonstrated the up-regulation of caspase-3 and caspase-7 genes in C2C12 cells after treatment with Au-NPs. Reactive Oxygen Species 39-42 caspase 3 Mus musculus 164-173 24412703-7 2014 Blocking ROS generation using the antioxidant N-acetyl-l-cysteine abolished the apoptosis and caspase-3 activities induced by POMC gene delivery and hypoxia. Reactive Oxygen Species 9-12 caspase 3 Mus musculus 94-103 23770272-0 2013 Hydrogen sulfide prevents OGD/R-induced apoptosis via improving mitochondrial dysfunction and suppressing an ROS-mediated caspase-3 pathway in cortical neurons. Reactive Oxygen Species 109-112 caspase 3 Mus musculus 122-131 23770272-4 2013 The pretreatment of N-acetyl-l-cysteine (NAC, an ROS scavenger) also prevents OGD/R-induced activation of caspase-3. Reactive Oxygen Species 49-52 caspase 3 Mus musculus 106-115 23770272-7 2013 These data suggest that H2S can protect against OGD/R-induced neuronal apoptosis through improving mitochondria dysfunction and suppressing an ROS-activated caspase-3 signaling pathway. Reactive Oxygen Species 143-146 caspase 3 Mus musculus 157-166 22474074-7 2012 In turn, the abnormal ROS levels in the hippocampus of DA-treated mice activated SAPK/JNK pathway, decreased FoxO1 phosphorylation, stimulated the nuclear translocation of FoxO1, activated FasL/Fas signaling, and promoted the activation of caspase-8 and caspase-3, which resulted in neuron apoptosis and cognitive deficits in mice. Reactive Oxygen Species 22-25 caspase 3 Mus musculus 254-263 23928855-6 2013 In response to oxidative stress, the production of intracellular reactive oxygen species was significantly enhanced in TDAG51-deficient MEFs, resulting in the activation of caspase-3. Reactive Oxygen Species 65-88 caspase 3 Mus musculus 173-182 22815507-7 2012 Furthermore, concurrent increases in reactive oxygen species and nitric oxide production leading to increased caspase 3 activation are also observed in both murine and human microglial cells. Reactive Oxygen Species 37-60 caspase 3 Mus musculus 110-119