PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33292140-8 2021 Treatment with combination of 2.5 mM VPA and 3.12 muM Cu(II) complex induces oxidative stress in a time-dependent manner, as well as apoptosis that is evidenced by the increase in caspase 3/7 activity, positive annexin-V-FITC, and increase in M30 levels. Valproic Acid 37-40 caspase 3 Homo sapiens 180-191 27956235-7 2017 And we also observed that VPA up-regulated the active caspase-3 and Bcl-2/Bax ratio and inhibited cytochrome c (Cyt c) release from mitochondria to the cytoplasm. Valproic Acid 26-29 caspase 3 Homo sapiens 54-63 32167238-9 2020 These novel findings indicate that VPA may be capable of protecting the SH-SY5Y dopaminergic neuronal cells from 6-OHDA-induced toxicity via the deceasing of apoptotic caspases (cleaved caspase-3, caspase-7, and caspase-9) and reducing of the Bax/Bcl2 ratio. Valproic Acid 35-38 caspase 3 Homo sapiens 186-195 32456093-5 2020 The apoptosis associated noncleaved and cleaved caspase 3, and caspases were increased by exposure to VPA, which up-regulated cyclooxygenase 2 (COX-2) mRNA and protein levels likely through histone acetylation. Valproic Acid 102-105 caspase 3 Homo sapiens 48-57 32456093-6 2020 The COX-2 inhibitor NS-398 attenuated the effects of VPA up-regulating COX-2 expression and decreased VPA-induced caspase 3 expression. Valproic Acid 53-56 caspase 3 Homo sapiens 114-123 32456093-6 2020 The COX-2 inhibitor NS-398 attenuated the effects of VPA up-regulating COX-2 expression and decreased VPA-induced caspase 3 expression. Valproic Acid 102-105 caspase 3 Homo sapiens 114-123 32719967-5 2021 Mechanically, VPA boosted cellular apoptosis and cell-cycle arrest by increased level of cleaved caspase-3/caspase-3, cleaved PARP/PARP and Bax/Bcl-2. Valproic Acid 14-17 caspase 3 Homo sapiens 97-106 32719967-5 2021 Mechanically, VPA boosted cellular apoptosis and cell-cycle arrest by increased level of cleaved caspase-3/caspase-3, cleaved PARP/PARP and Bax/Bcl-2. Valproic Acid 14-17 caspase 3 Homo sapiens 107-116 28160167-5 2017 RESULTS: We found that both VPA and TSA can induce apoptosis in Panc1 and PaCa44 pancreatic cancer-derived cells by triggering mitochondrial membrane depolarization, Cytochrome c release and Caspase 3 activation, although VPA was more effective than TSA, especially in Panc1 cells. Valproic Acid 28-31 caspase 3 Homo sapiens 191-200 28055238-3 2017 VPA treatment (1.5, 3.0, or 4.5 mM) altered (p < 0.05) the growth characteristics and relative expression level of HDAC1, DNMT1, DNMT3a, P53, and CASPASE3, and the global level of H3K9/14ac, H4K5ac, and H3K18ac but not H3K27me3 in the cells. Valproic Acid 0-3 caspase 3 Homo sapiens 149-157 27627801-8 2016 On treatment with VPA and cytostatics, CD133+ cells were mainly detected in the S and G2/M phases of the cell cycle and they showed less activated caspase-3 compared to CD133- cells. Valproic Acid 18-21 caspase 3 Homo sapiens 147-156 27654264-6 2016 RESULTS: Paclitaxel and DOX decreased cell viability and increased caspase-3 activity, and co-treatment with VPA enhanced this effect. Valproic Acid 109-112 caspase 3 Homo sapiens 67-76 25745763-6 2014 Simultaneously, it was observed that VPA at higher concentrations (5 and 10 mM) caused an increase in caspase-3 activity. Valproic Acid 37-40 caspase 3 Homo sapiens 102-111 21176348-5 2010 The expressions of anti-apoptotic protein BCL-2 and h-tert mRNA were significantly decreased while the pro-apoptotic protein BAX and caspase-3 activity increased after treatment with VPA. Valproic Acid 183-186 caspase 3 Homo sapiens 133-142 23918508-6 2013 VPA enhanced the cleavage of caspase-3 and caspase-9 in A549 cells cocultured with gammadelta T cells, and such enhancement was reversed by the MICA antibody. Valproic Acid 0-3 caspase 3 Homo sapiens 29-38 23389658-8 2013 Our results showed that either VPA-induced alpha-Syn upregulation or addition of recombinant alpha-Syn protect primary cortical neurons from soluble Abeta1-42 decreasing the caspase-3-mediated cell death. Valproic Acid 31-34 caspase 3 Homo sapiens 174-183 21933621-4 2011 Sodium valproate-induced apoptosis in HepG2 cells was investigated with fluorescence microscopy to detect morphological changes; by flow cytometry to calculate DNA ploidy and apoptotic cell percentages; with Western blotting analyses to determine c-Jun N-terminal kinases (JNK), p-JNK, Bcl-2, Bax, and caspase-3 and -9 protein expression levels; and using JC-1 fluorescence microscopy to detect the membrane potential of mitochondria. Valproic Acid 0-16 caspase 3 Homo sapiens 302-318 24918603-4 2014 Dasatinib was found to exert potent synergistic inhibitory effects on VPA-treated AML cells in association with G1 phase cell cycle arrest and apoptosis induction involving the cleavage of poly (ADP-ribose) polymerase and caspase-3, -7 and -9. Valproic Acid 70-73 caspase 3 Homo sapiens 222-242 23097134-4 2013 Using human neuroblastoma cell lines, SK-N-MC, SH-SY5Y, and SK-N-SH, we show that non-toxic dose (2 mM) of VPA enhanced staurosporine (STS)-induced cell death as assessed by MTT assay, PARP cleavage, hypodiploidy, and caspase 3 activity. Valproic Acid 107-110 caspase 3 Homo sapiens 218-227 22814014-5 2012 Time-dependent effects of VPA and LEV on activity of caspases (-3, -8 and -9) activity were evaluated by fluorescent assay and western blotting. Valproic Acid 26-29 caspase 3 Homo sapiens 53-76 21507255-10 2011 In addition, the results of our caspase 3 activation studies demonstrated that prior treatment with VPA increased the anticancer drug cisplatin-induced activation of caspase 3 in both HTB4 and HTB9 cells. Valproic Acid 100-103 caspase 3 Homo sapiens 32-41 21507255-10 2011 In addition, the results of our caspase 3 activation studies demonstrated that prior treatment with VPA increased the anticancer drug cisplatin-induced activation of caspase 3 in both HTB4 and HTB9 cells. Valproic Acid 100-103 caspase 3 Homo sapiens 166-175 20568898-3 2010 In undifferentiated cells, the cytotoxicity of both butyrate and valproate was associated with activation of the intrinsic apoptotic pathway since we observed dissipation of mitochondrial membrane potential, induction of caspase-9 and caspase-3 activities, appearance of sub-G1 DNA and loss of plasma membrane asymmetry and/or integrity. Valproic Acid 65-74 caspase 3 Homo sapiens 235-244 20889917-7 2010 Cytarabine and VPA cooperatively induced DNA double-strand breaks, reflected in induction of gammaH2AX and apoptosis, accompanied by activation of caspase-9 and caspase-3. Valproic Acid 15-18 caspase 3 Homo sapiens 161-170 20811699-2 2010 The present study showed that the histone deacetylase (HDAC) inhibitors valproic acid (VPA) and depsipeptide (FK228) synergistically enhanced ionizing radiation (IR)-induced apoptosis, associated with activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase in Y79 and WER1-Rb1 human retinoblastoma cells. Valproic Acid 72-85 caspase 3 Homo sapiens 215-224 20811699-2 2010 The present study showed that the histone deacetylase (HDAC) inhibitors valproic acid (VPA) and depsipeptide (FK228) synergistically enhanced ionizing radiation (IR)-induced apoptosis, associated with activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase in Y79 and WER1-Rb1 human retinoblastoma cells. Valproic Acid 87-90 caspase 3 Homo sapiens 215-224 16678157-3 2006 Pretreatment of SH-SY5Y cells for 7 days, but not 1 day, with 1 mM of lithium or 0.6 mM of valproate significantly reduced rotenone and H2O2-induced cytotoxicity, cytochrome c release and caspase-3 activation, and increased Bcl-2 levels. Valproic Acid 91-100 caspase 3 Homo sapiens 188-197 16849572-8 2006 However, when VPA is chronically administered (10-14 days) to prostate cancer cells, even lower doses of VPA result in marked decreases in the net proliferation rate, correlating with increased caspase-2 and caspase-3 activation. Valproic Acid 14-17 caspase 3 Homo sapiens 208-217 17534580-10 2007 Finally, a significant increase in caspase-3 activity and apoptosis was observed in the presence of both VPA and etoposide compared to either agent alone. Valproic Acid 105-108 caspase 3 Homo sapiens 35-44 17273758-9 2007 Since caspase 3 is activated in all tested cell lines after VPA treatment, a caspase-dependent pathway seems to be involved but not activated by the classic apoptotic pathways. Valproic Acid 60-63 caspase 3 Homo sapiens 6-15 16412349-15 2005 After treatment with VPA, the level of caspase 3 in U937 increased from (14.09 +/- 1.19)% to (32.30 +/- 2.47)%, and caspase 8 from (4.58 +/- 1.41)% to (86.47 +/- 3.26)% (P < 0.01), but there was no significant change in caspase 9 [(13.25 +/- 3.11)% and (10.95 +/- 1.30)%]. Valproic Acid 21-24 caspase 3 Homo sapiens 39-48 16412349-19 2005 CONCLUSION: VPA could induce apoptosis of U937 through the activation of caspase 3 and 8; and it induced the apoptosis of Jurkat involving the activation of caspase 3 and 9. Valproic Acid 12-15 caspase 3 Homo sapiens 73-82 16412349-19 2005 CONCLUSION: VPA could induce apoptosis of U937 through the activation of caspase 3 and 8; and it induced the apoptosis of Jurkat involving the activation of caspase 3 and 9. Valproic Acid 12-15 caspase 3 Homo sapiens 157-166 11072136-0 2000 A novel evidence of different mechanisms of lithium and valproate neuroprotective action on human SY5Y neuroblastoma cells: caspase-3 dependency. Valproic Acid 56-65 caspase 3 Homo sapiens 124-133 12721699-7 2003 In an 18-year-old boy, who suffered from valproic acid-associated acute hepatitis, caspase-3 cells were clustered among the necrotic foci and the foamy cells. Valproic Acid 41-54 caspase 3 Homo sapiens 83-92 11916526-3 2002 VPA-treatment induced apoptotic changes in MV411 cells including DNA fragmentation, phosphatidylserine externalization, cytochrome c release from mitochondria, and activation of caspases-3, -8, and -9. Valproic Acid 0-3 caspase 3 Homo sapiens 178-200