PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30091676-8 2019 In addition, intracellular ROS, cleaved caspase-3, Bax:Bcl-2 ratio, and cytochrome c release were significantly increased in 6-OHDA-incubated cells. Oxidopamine 125-131 caspase 3 Homo sapiens 40-49 31685899-6 2019 Furthermore, NAPE-PLD silencing protects cathecolamine-producing SH-SY5Y cells from 6-OHDA-induced reactive oxygen species formation, caspase-3 activation and death. Oxidopamine 84-90 caspase 3 Homo sapiens 134-143 33999357-3 2021 PME also blocked several 6-OHDA-induced mitochondrial apoptotic cascades, including loss of mitochondrial membrane potential, caspase 3 and PARP activation, and a decrease in the Bcl-2/Bax ratio. Oxidopamine 25-31 caspase 3 Homo sapiens 126-135 30053409-3 2018 The pretreatment of SH-SY5Y cells with HT-B, but not HT or HT-A significantly reduced the 6-OHDA-induced generation of reactive oxygen species, activation of caspase-3, and subsequent cell death. Oxidopamine 90-96 caspase 3 Homo sapiens 158-167 30128145-6 2018 The inhibition of beta5i further promoted the activation of Caspase 3-related pathways induced by 6-OHDA. Oxidopamine 98-104 caspase 3 Homo sapiens 60-69 28782414-9 2018 Data showed that 6-OHDA could decrease cell viability and mitochondrial membrane potential and increase intracellular ROS, cytochrome c, and cleaved caspase-3 levels. Oxidopamine 17-23 caspase 3 Homo sapiens 149-158 29671234-8 2018 6-OHDA exposure was up-regulated caspase-3 and Keap-1 and, down-regulated Nrf2, BDNF and p-CREB, which were sufficiently reverted by gallic acid pre-treatment. Oxidopamine 0-6 caspase 3 Homo sapiens 33-42 29429149-6 2018 CORM-2 treatment decreased Bax/Bcl2 ratio and caspase-3 activity, which had been increased by 6-OHDA. Oxidopamine 94-100 caspase 3 Homo sapiens 46-55 29079356-11 2018 6-OHDA exposure increased the expression of the transcription factor c-JUN, increased the expression of the mitochondria maintenance Phosphatase and tensin homologue-induced putative kinase 1 (PINK1) protein and increased the expression of pro-apoptotic PUMA, caspase-3 and apoptosis-inducing factor (AIF). Oxidopamine 0-6 caspase 3 Homo sapiens 260-269 29444677-6 2018 The data suggest that the cell death induced by 6-OHDA was mediated by an increase of H2O2 production, the depolarization of mitochondrial membrane potential and the increase of Caspase-3 activity. Oxidopamine 48-54 caspase 3 Homo sapiens 178-187 29204750-7 2018 Moreover, fisetin effectively suppressed 6-OHDA-mediated activation of caspase-3 and caspase-9, which leads to the cell death, while, 6-OHDA-induced caspase-3/7 activity was lowered. Oxidopamine 41-47 caspase 3 Homo sapiens 71-80 29204750-7 2018 Moreover, fisetin effectively suppressed 6-OHDA-mediated activation of caspase-3 and caspase-9, which leads to the cell death, while, 6-OHDA-induced caspase-3/7 activity was lowered. Oxidopamine 134-140 caspase 3 Homo sapiens 149-158 28543594-6 2018 In addition, PC12 or SH-SY5Y cells were treated with miR-124-3p mimics or inhibitors following 6-OHDA administration, which mediated cell apoptosis and downregulation or upregulation of Caspase-3 activity, respectively. Oxidopamine 95-101 caspase 3 Homo sapiens 186-195 26773499-6 2016 6-OHDA-induced intracellular generation of ROS and mitochondrial dysfunctions, release of cytochrome c, imbalance of Bax/Bcl-2, cleaved caspase-9/caspase-9 and cleaved caspase-3/caspase-3 ratio, and p-p53 activation were strikingly attenuated by SJP pretreatment. Oxidopamine 0-6 caspase 3 Homo sapiens 168-177 28534853-4 2017 Results from in vitro experiments show that 1T3O effectively inhibits 6-hydroxydopamine-induced (6-OHDA-induced) activation of both p38 mitogen-activated protein kinase (MAPK) and caspase-3 in SH-SY5Y cells; and enhances nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression via phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling. Oxidopamine 70-87 caspase 3 Homo sapiens 180-189 28534853-4 2017 Results from in vitro experiments show that 1T3O effectively inhibits 6-hydroxydopamine-induced (6-OHDA-induced) activation of both p38 mitogen-activated protein kinase (MAPK) and caspase-3 in SH-SY5Y cells; and enhances nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression via phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling. Oxidopamine 97-103 caspase 3 Homo sapiens 180-189 27091487-6 2016 In cells pretreated with the proteasome inhibitor MG132, CA no longer reversed the 6-OHDA-mediated induction of cleavage of caspase 3 and poly(ADP)-ribose polymerase and no longer reversed the suppression of proteasome activity. Oxidopamine 83-89 caspase 3 Homo sapiens 124-165 26773499-6 2016 6-OHDA-induced intracellular generation of ROS and mitochondrial dysfunctions, release of cytochrome c, imbalance of Bax/Bcl-2, cleaved caspase-9/caspase-9 and cleaved caspase-3/caspase-3 ratio, and p-p53 activation were strikingly attenuated by SJP pretreatment. Oxidopamine 0-6 caspase 3 Homo sapiens 178-187 25818191-6 2015 Also, DHC inhibited the expression of activated caspase-3 and caspase-9 and cleaved PARP in 6-OHDA-induced SH-SY5Y cells. Oxidopamine 92-98 caspase 3 Homo sapiens 48-57 27298749-11 2016 Hepcidin knockdown also reduced 6-OHDA induced caspase-3 activity by 42% (P < 0.05) and DNA fragmentation by 29% (P = 0.086) and increased cell viability by 22% (P < 0.05). Oxidopamine 32-38 caspase 3 Homo sapiens 47-56 26904174-7 2015 RESULTS: The data showed that 6-OHDA caused significant cell damage, loss of mitochondrial membrane potential and increase in intracellular reactive oxygen species and calcium levels as well as activated caspase-3 and cytochrome-c release. Oxidopamine 30-36 caspase 3 Homo sapiens 204-213 26033682-5 2015 6-OHDA-induced dysfunctions, including the decrease of mitochondrial membrane potential (DeltaPsim), increase of intracellular free Ca(2+), imbalance of Bcl-2/Bax ratio, release of Cyt-c from the mitochondria and activation of caspase-3 and caspase-9 were attenuated by CS pretreatment, which demonstrated that CS suppressed 6-OHDA-induced apoptosis in SH-SY5Y cells possibly through mitochondria protection. Oxidopamine 0-6 caspase 3 Homo sapiens 227-236 23940672-0 2013 Activation of GSK-3beta and caspase-3 occurs in Nigral dopamine neurons during the development of apoptosis activated by a striatal injection of 6-hydroxydopamine. Oxidopamine 145-162 caspase 3 Homo sapiens 28-37 23958447-6 2014 Furthermore, AMS36 reversed 6-OHDA-induced loss of tyrosine hydroxylase and attenuated 6-OHDA-induced activation of caspase-3, triggering apoptosis, intracellular generation of reactive oxygen species and mitochondrial dysfunction, including the release of cytochrome c and an imbalanced Bax/Bcl-2 ratio. Oxidopamine 87-93 caspase 3 Homo sapiens 116-125 24390959-8 2014 Furthermore, EPO increased the expression of phosphorylated Akt and phosphorylated FoxO3a, and abrogated the 6-OHDA-induced dysregulation of Bcl-2, Bax and Caspase-3 in PC12 cells and in striatal neurons. Oxidopamine 109-115 caspase 3 Homo sapiens 156-165 24341565-10 2014 In addition, intracellular ROS and calcium levels, activated caspase-3, Bax:Bcl-2 ratio, cytochrome c release, as well as DNA fragmentation were significantly increased in 6-OHDA-treated cells. Oxidopamine 172-178 caspase 3 Homo sapiens 61-70 23857913-0 2014 Curcumin I mediates neuroprotective effect through attenuation of quinoprotein formation, p-p38 MAPK expression, and caspase-3 activation in 6-hydroxydopamine treated SH-SY5Y cells. Oxidopamine 141-158 caspase 3 Homo sapiens 117-126 24135219-10 2013 In addition, intracellular ROS, activated caspase 3, Bax/Bcl-2 ratio, cytochrome c as well as DNA fragmentation were significantly increased in 6-OHDA-treated cells. Oxidopamine 144-150 caspase 3 Homo sapiens 42-51 23940672-2 2013 This work evaluated whether a single striatal injection of 6-OHDA causes progressive apoptosis of dopamine (DA) neurons and activation of glycogen synthase kinase 3beta (GSK-3beta) and caspase-3 in the substantia nigra compacta (SNc). Oxidopamine 59-65 caspase 3 Homo sapiens 185-194 23940672-12 2013 Our results suggest that caspase-3 and GSK-3beta pY216 activation might participate in the DA cell death and that the active caspase-3 might also participate in the neuroinflammation caused by the striatal 6-OHDA injection. Oxidopamine 206-212 caspase 3 Homo sapiens 125-134 20374430-7 2010 In the presence of 6-hydroxydopamine, GLP-1"s ability to lower caspase-3 activity was abolished with the phosphoinositide 3-kinase inhibitor, LY2940002, and partly reduced with the protein kinase A inhibitor, H89. Oxidopamine 19-36 caspase 3 Homo sapiens 63-72 22894569-4 2012 CA at 1 muM suppressed the 6-OHDA-induced nuclear condensation, reactive oxygen species generation, and cleavage of caspase 3 and PARP. Oxidopamine 27-33 caspase 3 Homo sapiens 116-125 22119889-8 2012 The pharmacological activity of this compound has been studied, and it is associated with the inhibition of 6-OHDA-induced activation of caspase-3 and translocation of nuclear factor kappa B. Oxidopamine 108-114 caspase 3 Homo sapiens 137-146 21397656-6 2011 6-OHDA-induced nitrosative stress ultimately caused apoptotic cell death as determined by decreased Bcl-2/Bax ratio, activation of c-Jun N-terminal kinase (JNK), and cleavage of caspase-3 and poly(ADP-ribose)polymerase (PARP), which were attenuated by peroxynitrite decomposition catalyst, 5,10,15,20-tetrakis(4-sulfonatophenyl)prophyrinato iron(III) (FeTPPS). Oxidopamine 0-6 caspase 3 Homo sapiens 178-187 23286644-8 2013 6-OHDA treatment induced an accumulation of reactive oxygen species, an increase of the expression of the pro-apoptotic gene Bax, a drop of the mitochondrial membrane potential and a stimulation of caspase-3 activity. Oxidopamine 0-6 caspase 3 Homo sapiens 198-207 23540413-0 2013 Caspase-2 and caspase-8 trigger caspase-3 activation following 6-OHDA-induced stress in human dopaminergic neurons differentiated from ReNVM stem cells. Oxidopamine 63-69 caspase 3 Homo sapiens 32-41 22538490-5 2012 Moreover, when compared to wild-type DA neurons, LRRK2-G2019S iPSC-derived DA neurons were more sensitive to caspase-3 activation caused by exposure to hydrogen peroxide, MG-132, and 6-hydroxydopamine. Oxidopamine 183-200 caspase 3 Homo sapiens 109-118 22160861-5 2012 Exposure to 6-OHDA did not affect hMSCs, but induced DAT-independent apoptosis in mdNSCs with generation of reactive oxygen species and caspases 3/7 activation. Oxidopamine 12-18 caspase 3 Homo sapiens 136-148 22200816-6 2012 In this study, we found that pretreatment with SF significantly reduced 6-OHDA-induced caspase-3 activation and subsequent cell death. Oxidopamine 84-90 caspase 3 Homo sapiens 99-108 20920551-5 2011 We found that 6-OHDA increased the expression of caspase-3 and caspase-9 but not caspase-8. Oxidopamine 14-20 caspase 3 Homo sapiens 49-58 20920551-7 2011 Moreover, 6-OHDA induced less cell viability loss and lower expression of caspase-9 and caspase-3 in GSK3beta knockdown group compared with control. Oxidopamine 10-16 caspase 3 Homo sapiens 88-97 20708055-6 2010 6-OHDA-induced intracellular generation of reactive oxygen species (ROS), activation of p38 MAPK and ERK1/2, and mitochondrial dysfunctions, including the decrease of membrane potential, increase of intracellular free Ca2+, release of cytochrome c, imbalance of Bax/Bcl-2 ratio and activation of caspase-3 were strikingly attenuated by chrysotoxine pretreatment. Oxidopamine 0-6 caspase 3 Homo sapiens 296-305 19443200-5 2010 Release of lactate dehydrogenase and activity of caspase-3 triggered by 6-OHDA were significantly reduced by resveratrol and one of the methylated derivatives, pinostilbene (3,4"-dihydroxy-5-methoxystilbene), in a dose-dependent manner. Oxidopamine 72-78 caspase 3 Homo sapiens 49-58 18554677-4 2008 Pretreatment of SH-SY5Y cells with MT-III significantly reduced 6-OHDA-induced generation of ROS, caspase-3 activation, and subsequent cell death. Oxidopamine 64-70 caspase 3 Homo sapiens 98-107 19781563-6 2010 Pretreatment of SH-SY5Y cells with Rb1 significantly reduced 6-OHDA-induced caspase-3 activation and subsequent cell death. Oxidopamine 61-67 caspase 3 Homo sapiens 76-85 19801972-4 2009 First, parkin prevented 6-hydroxydopamine-induced caspase-3 activation in a p53-dependent manner. Oxidopamine 24-41 caspase 3 Homo sapiens 50-59 19014378-6 2008 In addition, Asx strikingly inhibited 6-OHDA-induced mitochondrial dysfunctions, including lowered membrane potential and the cleavage of caspase 9, caspase 3, and poly(ADP-ribose) polymerase. Oxidopamine 38-44 caspase 3 Homo sapiens 149-158 18201823-6 2008 Caffeine lowered caspase-3 activity induced by serum/RA deprivation and 6-OHDA administration, and also decreased the number of apoptotic condensed and/or fragmented nuclei. Oxidopamine 72-78 caspase 3 Homo sapiens 17-26 18593583-2 2008 Pretreatment of SH-SY5Y cells with kahweol significantly reduced 6-OHDA-induced generation of ROS, caspase-3 activation, and subsequent cell death. Oxidopamine 65-71 caspase 3 Homo sapiens 99-108 17884684-6 2008 Salvianolic acid B reduced the 6-hydroxydopamine-induced increase of caspase-3 activity, and reduced cytochrome C translocation into the cytosol from mitochondria. Oxidopamine 31-48 caspase 3 Homo sapiens 69-78 17847117-8 2008 In contrast, activation of caspase-3 by 6-OHDA was delayed, occurring after about 6 hr, and this activation was increased by inhibition of the first phosphorylated ERK1/2 peak. Oxidopamine 40-46 caspase 3 Homo sapiens 27-36 15132987-8 2004 Blocking GSK3beta activity by selective inhibitors (lithium, TDZD-8, and L803-mts) prevented 6-OHDA-induced cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), DNA fragmentations and cell death. Oxidopamine 93-99 caspase 3 Homo sapiens 120-129 17975304-6 2007 Isoborneol protected against 6-OHDA-induced increases in caspase-3 activity and cytochrome C translocation into the cytosol from mitochondria. Oxidopamine 29-35 caspase 3 Homo sapiens 57-66 15894425-8 2005 Caspase-3 activation following 6-OHDA treatment was markedly inhibited in the presence of CAPE. Oxidopamine 31-37 caspase 3 Homo sapiens 0-9 15030396-8 2004 Herein, we present evidence supporting that the Bcl-x(L)-anti-apoptotic signal pathway seems to prevent mitochondrial multiple conductance channel opening, cytochrome c release and caspase-3 like activity following 6-OHDA treatment in the human neuroblastoma cell line SH-SY5Y. Oxidopamine 215-221 caspase 3 Homo sapiens 181-190 33808343-6 2021 Treatment of differentiated SH-SY5Y cells with 6-OHDA brought cell death, and specifically, apoptosis, which was significantly inhibited by the preincubation with MJe through caspase 3 blockage and the modulation of p53, Bax, and Bcl-2 genes. Oxidopamine 47-53 caspase 3 Homo sapiens 175-184