PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23441212-7 2013 Furthermore, the inhibition of autophagy also stimulated ROS formation and scavenging of ROS by antioxidant NAC inhibited caspase-3 activity, prevented the release of cyt-c from mitochondria and eventually rescued cancer cells from 5-FU-mediated apoptosis. ros 89-92 caspase 3 Homo sapiens 122-131 25308836-8 2014 Scavenging of ROS by antioxidant N-acetyl-cysteine (NAC) inhibited caspase-3 activity and rescued the cells from apoptosis. ros 14-17 caspase 3 Homo sapiens 67-76 25064160-5 2014 Interestingly, quenching of ROS with tiron, an antioxidant, offered significant protection against HC-induced inhibition of cell growth and down regulation of caspase-3, suggesting the crucial role of ROS in mediating cell death. ros 28-31 caspase 3 Homo sapiens 159-168 25064160-5 2014 Interestingly, quenching of ROS with tiron, an antioxidant, offered significant protection against HC-induced inhibition of cell growth and down regulation of caspase-3, suggesting the crucial role of ROS in mediating cell death. ros 201-204 caspase 3 Homo sapiens 159-168 24586814-7 2014 Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis. ros 14-17 caspase 3 Homo sapiens 146-155 23688756-13 2013 CONCLUSION: Mechanisms underlying bone marrow damage by iron overload might be through the follows: (1)The increased ROS induced by excessive iron deposition affected the expressions of Caspase-3 and Bcl-2, which caused more BMMNC apoptosis; (2)The abnormal number and ratio of T lymphocytes caused by iron overload aggravated the abnormality of immunity of IRP; (3)Iron overload may increase the damage to erythrocytes and stem cells coated with auto-antibodies. ros 117-120 caspase 3 Homo sapiens 186-195 24717093-6 2014 The increase in ROS production then triggers caspase-3 activation resulting in the inhibition of long-term potentiation. ros 16-19 caspase 3 Homo sapiens 45-54 24077485-3 2013 ROS formation and changes in mitochondrial transmembrane potential may have influenced caspase-3 activation, a crucial enzyme in the apoptotic process. ros 0-3 caspase 3 Homo sapiens 87-96 23529952-5 2013 Results indicate that PEG2000-DPSE-QUE-NPS showed dose-dependent cytotoxicity to C6 glioma cells and enhanced ROS accumulation induced upregulation of p53 protein, which was accompanied with an increase in cytochrome c and caspase-3 protein levels. ros 110-113 caspase 3 Homo sapiens 223-232 23769964-11 2013 In conclusion, the study highlights ROS mediated DNA damage, lysosomal and mitochondrial destabilization via upregulation of Bax and activation of caspase-3 which further leads to apoptosis. ros 36-39 caspase 3 Homo sapiens 147-156 23834359-6 2013 We also demonstrate that caspase-3-deficient MEFs are less sensitive to intrinsic cell death stimulation, yet have higher ROS production. ros 122-125 caspase 3 Homo sapiens 25-34 23834359-9 2013 After activation by caspase-9, caspase-3 inhibits ROS production and is required for efficient execution of apoptosis, while effector caspase-7 is required for apoptotic cell detachment. ros 50-53 caspase 3 Homo sapiens 31-40 21453688-4 2011 An increase in the intracellular ROS level by EPO1 was observed in the DCHF-DA analysis, and EPO1-induced apoptosis and caspase 3 protein cleavage were prevented by adding the antioxidant, N-acetyl-cysteine (NAC), with decreased ROS production elicited by EPO1. ros 229-232 caspase 3 Homo sapiens 120-129 22739161-6 2012 The positive cell number of activated caspase 3, caspase 8, caspase 9 and the levels of activated caspase 3, caspase 9, p-JNK, P38 increased after Jurkat cells were treated with GA. ROS, CaMKII, caspase 3, caspase 9, MAPKK, JNK1/2 and P38 inhibitors had some significant effect on GA-induced apoptosis. ros 182-185 caspase 3 Homo sapiens 98-107 22739161-6 2012 The positive cell number of activated caspase 3, caspase 8, caspase 9 and the levels of activated caspase 3, caspase 9, p-JNK, P38 increased after Jurkat cells were treated with GA. ROS, CaMKII, caspase 3, caspase 9, MAPKK, JNK1/2 and P38 inhibitors had some significant effect on GA-induced apoptosis. ros 182-185 caspase 3 Homo sapiens 98-107 22739161-7 2012 ROS, CaMKII, MAPKK, JNK1/2 and P38 inhibitors decreased the levels of activated caspase 3, caspase 9 by GA.ROS, CaMKII, MAPKK, JNK1/2 inhibitors decreased the levels of p-JNK by GA. ROS, CaMKII, MAPKK, P38 inhibitors decreased the levels of P38 by GA. ros 0-3 caspase 3 Homo sapiens 80-89 22739161-7 2012 ROS, CaMKII, MAPKK, JNK1/2 and P38 inhibitors decreased the levels of activated caspase 3, caspase 9 by GA.ROS, CaMKII, MAPKK, JNK1/2 inhibitors decreased the levels of p-JNK by GA. ROS, CaMKII, MAPKK, P38 inhibitors decreased the levels of P38 by GA. ros 107-110 caspase 3 Homo sapiens 80-89 22739161-7 2012 ROS, CaMKII, MAPKK, JNK1/2 and P38 inhibitors decreased the levels of activated caspase 3, caspase 9 by GA.ROS, CaMKII, MAPKK, JNK1/2 inhibitors decreased the levels of p-JNK by GA. ROS, CaMKII, MAPKK, P38 inhibitors decreased the levels of P38 by GA. ros 107-110 caspase 3 Homo sapiens 80-89 21982843-0 2011 Plumbagin and juglone induce caspase-3-dependent apoptosis involving the mitochondria through ROS generation in human peripheral blood lymphocytes. ros 94-97 caspase 3 Homo sapiens 29-38 18243471-3 2008 The increased ROS by cerium oxide nanoparticles triggered the activation of cytosolic caspase-3 and chromatin condensation, which means that cerium oxide nanoparticles exert cytotoxicity by an apoptotic process. ros 14-17 caspase 3 Homo sapiens 86-95 21543583-5 2011 IL-12 treatment induces NK cell activation as well as levels of ROS, but prolonged IL-12 treatment causes ROS accumulation, which in turn, results in the loss of Deltapsi(m), the release of cytochrome c, and the activation of caspase-3, resulting in NK cell apoptosis. ros 106-109 caspase 3 Homo sapiens 226-235 21624350-6 2011 Moreover, when the free radical (ROS) generating capacity of the compounds was studied by 2",7"-dichlorofluorescein-diacetate assay using flow cytometry, we found that a known antioxidant N-acetyl-cysteine almost completely abrogated the H2AX((S139)) phosphorylations and the caspase 3 cleavage and activation. ros 33-36 caspase 3 Homo sapiens 276-285 20940027-5 2011 Furthermore, western blot analysis of p53, JNK, and caspase-3 showed that ROS generation was accompanied by JNK activation. ros 74-77 caspase 3 Homo sapiens 52-61 20512627-10 2010 The ROS scavenger NAC efficiently suppressed not only ROS generation, but also caspase-3-mediated PARP cleavage, apoptosis, and release of cytochrome c and AIF, indicating a role of ROS in combined Dox + DMPS treatment-induced apoptotic death signaling. ros 4-7 caspase 3 Homo sapiens 79-88 18385754-7 2008 We further showed that the ROS-induced degradation of BCR-ABL was mediated partially by caspase-3 and the proteasome pathway. ros 27-30 caspase 3 Homo sapiens 88-97 20846705-8 2010 These results suggest that the translocation of PKC-delta was mediated by ROS-dependent caspase-3 activity. ros 74-77 caspase 3 Homo sapiens 88-97 20846705-10 2010 Taken together, this study suggests that ROS generation is an upstream event for TCDD-induced chondrocyte apoptosis and PKC-delta mediates the apoptotic processes through ROS-dependent caspase-3 activation. ros 171-174 caspase 3 Homo sapiens 185-194 19815061-6 2010 With the generation of ROS, the increased activity of caspase-3 was shown, and was followed by chromatin condensation and breakage, which is an indication of the cellular apoptotic process. ros 23-26 caspase 3 Homo sapiens 54-63 33785100-6 2021 The results proved the presence of ROS that triggered the intrinsic apoptotic pathway, which was confirmed through a decrease in (Bcl-2), the release of cytochrome c, activation of caspase-9, and caspase-3. ros 35-38 caspase 3 Homo sapiens 196-205 18064039-4 2008 In addition, the data reveal that gzmB(+)CTL independently induce pro-apoptotic processes either via caspase-3/-7, leading to plasma membrane perturbance and ROS production or via Bid/Bak/Bax, resulting in cytochrome c release and that both pathways elicit loss of DeltaPsi(m). ros 158-161 caspase 3 Homo sapiens 101-113 18001034-6 2007 Berberine also inhibited the generation of ROS and the subsequent mitochondrial membrane potential collapse, chromosome condensation, cytochrome C release, and caspase-3 activation induced by oxLDL in HUVECs. ros 43-46 caspase 3 Homo sapiens 160-169 12880425-5 2003 Generation of ROS and hyperpolarization of mitochondrial transmembrane potential (DeltaPsim) were early events, followed by increased Fas expression and activation of caspase-8, and then activation of caspase-3 and -9. ros 14-17 caspase 3 Homo sapiens 201-217 34510030-4 2021 These effects reflected caspase 3-mediated apoptosis and could be attenuated or abolished by inhibiting ROS production with N-acetyl-L-cysteine, inhibiting autophagy with chloroquine, or silencing ATG7 with targeted siRNA. ros 104-107 caspase 3 Homo sapiens 24-33 34571081-6 2021 While high levels of ROS caused activation of caspase-3 and GSDME, and induced cell pyroptosis. ros 21-24 caspase 3 Homo sapiens 46-55 34834392-9 2021 Moreover, ZnONPs also enhanced ROS production which led to a significant loss of mitochondrial membrane potential and activated caspase-3 gene expression and caspase-3/7 activity in human hepatocellular carcinoma (HepG2) cells. ros 31-34 caspase 3 Homo sapiens 128-137 34834392-9 2021 Moreover, ZnONPs also enhanced ROS production which led to a significant loss of mitochondrial membrane potential and activated caspase-3 gene expression and caspase-3/7 activity in human hepatocellular carcinoma (HepG2) cells. ros 31-34 caspase 3 Homo sapiens 158-169 34681952-11 2021 In the case of anti-cancerous activities, the lowest viability (23.45 +- 1.40%) with enhanced ROS/NOS production led to a significant disruption of mitochondrial membrane potential and greater caspase-3/7 gene expression and activity by UV-C mediated bimetallic Ag-ZnONPs (0.1/0.5). ros 94-97 caspase 3 Homo sapiens 193-204 34137412-9 2021 The synergistic effect jointly caused a burst generation of mitochondrial ROS, which significantly down-regulated Bcl-2 protein expression, accelerated cytochrome c release and triggered a cascade of apoptosis-related proteins of Caspase-3 and Caspase-9. ros 74-77 caspase 3 Homo sapiens 230-239 34369076-0 2021 Caspase-3-mediated GSDME induced Pyroptosis in breast cancer cells through the ROS/JNK signalling pathway. ros 79-82 caspase 3 Homo sapiens 0-9 34369076-7 2021 Furthermore, DOX treatments induced intracellular accumulation of ROS, stimulated the phosphorylation of JNK, and Caspase-3 activation, subsequently. ros 66-69 caspase 3 Homo sapiens 114-123 34369076-8 2021 In conclusion, the study suggests that GSDME triggered DOX-induced pyroptosis in the caspase-3 dependent reactions through the ROS/JNK signalling pathway. ros 127-130 caspase 3 Homo sapiens 85-94 34060394-5 2022 Moreover, this agent induced ROS-mediated apoptosis by altering the expression of Bax, Bim, Caspase3, Bcl2, and XIAP. ros 29-32 caspase 3 Homo sapiens 92-100 34208283-11 2021 Tariquidar enhanced Dox cytotoxicity by increasing intracellular ROS production leading to caspase-3 mediated apoptosis. ros 65-68 caspase 3 Homo sapiens 91-100 33022360-9 2020 Restoration of physiological apoptosis by increasing the release of intracellular calcium to generate ROS thereby reducing the mitochondrial membrane potential for the release of cytochrome c and activation of caspase-3 was also reported with Imatinib administration. ros 102-105 caspase 3 Homo sapiens 210-219 33527955-0 2021 The main anthocyanin monomer of Lycium ruthenicum Murray induces apoptosis through the ROS/PTEN/PI3K/Akt/caspase 3 signaling pathway in prostate cancer DU-145 cells. ros 87-90 caspase 3 Homo sapiens 105-114 32146648-6 2020 Corroborating the above observations, we found that the ROS scavenger N-acetylcysteine (NAC) countered caspase-3 activity and the cells were rescued from apoptosis. ros 56-59 caspase 3 Homo sapiens 103-112 32948186-8 2020 The results of Annexin V-FITC/PI, JC-1, Western blot and ROS analysis showed that the expression of cleaved caspase-3 and Bax were up-regulated Bcl-2 was down-regulated in Cepharanthine or Curcumin treated groups, while ROS and MMP value were decreased at different degrees and the apoptosis rate was reduced. ros 57-60 caspase 3 Homo sapiens 108-117 32948186-8 2020 The results of Annexin V-FITC/PI, JC-1, Western blot and ROS analysis showed that the expression of cleaved caspase-3 and Bax were up-regulated Bcl-2 was down-regulated in Cepharanthine or Curcumin treated groups, while ROS and MMP value were decreased at different degrees and the apoptosis rate was reduced. ros 220-223 caspase 3 Homo sapiens 108-117 31277696-11 2019 Our results show that the antioxidative enzyme level and the ratio of Bcl-2/Bax decrease, the expression level of caspase 3 increases, the mitochondrial membrane potential is abnormal, and ROS accumulate in this system. ros 189-192 caspase 3 Homo sapiens 114-123 31030314-5 2020 One compound produces ROS which results in breast (MCF7) cancer cell death caused by apoptosis as evidenced by caspase 3/7 activation. ros 22-25 caspase 3 Homo sapiens 111-120 31250150-7 2020 Mitochondrial malfunction activates ROS signaling, which triggers caspase-3-mediated apoptosis of parietal cells. ros 36-39 caspase 3 Homo sapiens 66-75 31004300-5 2019 P2X7R, Bax, and Caspase-3 protein expression were detected by western blot and immunofluorescence analysis.The expression of P2X7R, ROS, Bax, and Caspase-3 in human podocytes incubated with oxLDL was significantly up-regulated and was found to have higher intracellular lipid accumulation and podocyte apoptosis compared with the NC group. ros 132-135 caspase 3 Homo sapiens 146-155 32107506-8 2020 The PVP-PdNPs generate continuous ROS in the mitochondria; this leads to the damage of the mitochondrial membrane potential and nuclear DNA and induces apoptosis through caspase3/7 enzymatic activity. ros 34-37 caspase 3 Homo sapiens 170-178 30777466-0 2019 Bufalin induces apoptosis via mitochondrial ROS-mediated caspase-3 activation in HCT-116 and SW620 human colon cancer cells. ros 44-47 caspase 3 Homo sapiens 57-66 30777466-12 2019 CONCLUSION: Bufalin significantly induces apoptosis in HCT-116 and SW620 colon cancer cells via mitochondrial ROS-mediated caspase-3 activation. ros 110-113 caspase 3 Homo sapiens 123-132 30196062-7 2018 Besides, 8 showed antiproliferative ability against NCI-H460 cells in a time- and concentration-dependent manner through modulating ROS to induce caspase-3-mediated pyroptosis, and displayed a better safety profile in vivo. ros 132-135 caspase 3 Homo sapiens 146-155 30125721-6 2018 The mechanism studies indicated the mitochondrial localization of BODIPY3-PEG3 was able to generate ROS in mitochondria, which further result in mitochondrial dysfunction and photoinduced apoptosis via caspase-8 and caspase-3 pathway. ros 100-103 caspase 3 Homo sapiens 216-225 29416349-0 2018 ROS-dependent Bax/Bcl2 and caspase 3 pathway-mediated apoptosis induced by zineb in human keratinocyte cells. ros 0-3 caspase 3 Homo sapiens 27-36 29940354-7 2018 A C60 fullerene photoactivation with violet light induced substantial ROS generation and apoptotic cell death, confirmed by caspase3/7 activation and plasma membrane phosphatidylserine externalization. ros 70-73 caspase 3 Homo sapiens 124-132 30111296-15 2018 Moreover, drug-loaded nano-cubosomes produced a notable escalation in ROS levels, evident as an increase in NADPH oxidase, inhibition of LDH and a consequential upsurge in caspase-3. ros 70-73 caspase 3 Homo sapiens 172-181 26152521-9 2016 Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells. ros 27-30 caspase 3 Homo sapiens 232-241 28591670-10 2017 Furthermore, altered levels of ROS triggers intrinsic apoptotic cascade, as evidenced by dissipated mitochondrial membrane potential (psi), decrease in Bcl-2/Bax ratio, cytochrome c release and cleavage of procaspase-3. ros 31-34 caspase 3 Homo sapiens 206-218 28417940-6 2017 The extract increased ROS production in HepG2 cells, which resulted in decreased GSH level, leading to apoptosis of these cells through activation of caspase-3 and caspase-7. ros 22-25 caspase 3 Homo sapiens 150-159 28138562-7 2017 Mitochondrial oxidative phosphorylation is inappropriately enhanced and, as a result of impaired electron transport and mitochondrial ROS increase, caspase-3 is activated and DNA damage is induced. ros 134-137 caspase 3 Homo sapiens 148-157 28592114-10 2017 However, pretreatment with N-acetyl- L-cysteine (NAC), a ROS scavenger, increased the expression of procaspase-3. ros 57-60 caspase 3 Homo sapiens 100-112 28636040-6 2017 Overproduction of ROS resulted in a strong decrease in the mitochondrial membrane potential, translocation of cytochrome c to the cytosol and activation of caspase 3, thus leading to apoptosis. ros 18-21 caspase 3 Homo sapiens 156-165 27888812-5 2017 SLNT induced apoptosis by activating Caspase-3 via both intrinsic and extrinsic pathways, which presented as the activation of Caspases-9 and -8, upregulation of cytochrome c and the Bax/Bcl-2 ratio, downregulation of NF-kappaB, and overproduction of ROS and TNF-alpha in vitro and in vivo. ros 251-254 caspase 3 Homo sapiens 37-46 26612416-8 2016 Moreover, Se@LDH-pooled siRNAs could induce cell apoptosis, change cell morphology and increase cellular ROS levels through change the expression of Bcl-2/Bax, activation of caspase-3, PI3K/AKT/mTOR and MAPK/ERK pathways. ros 105-108 caspase 3 Homo sapiens 174-183 26861955-4 2016 The statistically significant elevation of LDH levels, increased mitochondrial membrane potential, decreased ATP and increased ROS production, increased levels of DNA damage marker (8-OHdG) and activation of caspases: -3 and -9 confirmed by Real-Time PCR imply the activation of mitochondrial proapoptotic pathways induced by BZP after 24 h incubation. ros 127-130 caspase 3 Homo sapiens 208-227 25890231-9 2015 Cell apoptosis here is induced by following the ROS-mediated mitochondrial pathway, combined with downregulation of the expression levels of mRNA of XIAP and PARP-1 and upregulation of caspase3, Bcl-2 and Bcl-xL. ros 48-51 caspase 3 Homo sapiens 185-193 26549478-6 2015 ROS scavenger (N-acetyl cysteine, NAC) could attenuate both the resveratrol induced caspase-3 activity and the formation of acidic vacuoles, but failed to attenuate resveratrol induced PEL cell death. ros 0-3 caspase 3 Homo sapiens 84-93 25776488-7 2015 Combination with PA and IR also increased the production of ROS, which subsequently induced phosphorylation of p38, suppressed phosphorylation of ERK, and activated caspase-3, -8, and -9. ros 60-63 caspase 3 Homo sapiens 165-186