PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22222440-5 2012 In addition, fucoidan treatment inhibited apoptosis in H(2)O(2)-induced PC12 cells by increasing the Bcl-2/Bax ratio and decreasing active caspase-3 expression, as well as enhancing Akt phosphorylation (p-Akt). Hydrogen Peroxide 55-63 BCL2, apoptosis regulator Rattus norvegicus 101-106 21134432-10 2011 Western blot analysis indicated that pretreatment with Tan IIA prevented the increase in Bax/Bcl-2 ratio induced by H(2)O(2). Hydrogen Peroxide 116-124 BCL2, apoptosis regulator Rattus norvegicus 93-98 23221719-4 2012 The expression levels of pAkt/Akt, pErk/Erk, survivin, Bcl-2/Bax-alpha, and manganese-superoxide dismutase were increased by RSG pretreatment in H2O2-injured rat CMCs. Hydrogen Peroxide 145-149 BCL2, apoptosis regulator Rattus norvegicus 55-60 22927932-7 2012 The effect of ODN on the Bax/Bcl-2 balance contributed to abolish the deleterious action of H(2)O(2) on mitochondrial membrane integrity and caspase-3 activation. Hydrogen Peroxide 92-100 BCL2, apoptosis regulator Rattus norvegicus 29-34 21445859-7 2011 Moreover, cynaroside moderated H(2) O(2) -induced disruption of mitochondrial membrane potential, increased the expression of anti-apoptotic protein Bcl-2 while decreased the expression of pro-apoptotic protein Bax, and thereby inhibited the release of apoptogenic factors (cytochrome c and smac/Diablo) from mitochondria in H9c2 cells. Hydrogen Peroxide 31-40 BCL2, apoptosis regulator Rattus norvegicus 149-154 21478407-5 2011 In particular, H(2)O(2) preconditioning counteracted oxidative stress-induced apoptosis by decreasing caspase-3 activity, increasing Bcl2 expression and selectively increasing the expression and activity of antioxidant and phase II enzymes through Nrf1 and Nrf2 translocation to the nucleus. Hydrogen Peroxide 15-23 BCL2, apoptosis regulator Rattus norvegicus 133-137 21120620-2 2011 We have analyzed the apoptosis of H(2)O(2)-induced PC12 cells, H(2)O(2)-induced apoptosis appeared to correlate with lower Bcl-2 expression, higher Bax expression and sequential activation of caspase-3 leading to cleavage of poly-ADP-ribose polymerase (PARP). Hydrogen Peroxide 34-42 BCL2, apoptosis regulator Rattus norvegicus 123-128 21120620-2 2011 We have analyzed the apoptosis of H(2)O(2)-induced PC12 cells, H(2)O(2)-induced apoptosis appeared to correlate with lower Bcl-2 expression, higher Bax expression and sequential activation of caspase-3 leading to cleavage of poly-ADP-ribose polymerase (PARP). Hydrogen Peroxide 63-71 BCL2, apoptosis regulator Rattus norvegicus 123-128 21120620-4 2011 These results indicated that aucubin can obstruct H(2)O(2)-induced apoptosis by regulating of the expression of Bcl-2 and Bax, as well as suppression of caspases cascade activation. Hydrogen Peroxide 50-58 BCL2, apoptosis regulator Rattus norvegicus 112-117 22046407-13 2011 Our findings indicate that Tbeta4 selectively targets and upregulates catalase, Cu/Zn-SOD and Bcl(2), thereby, preventing H(2)O(2)-induced profibrotic changes in the myocardium. Hydrogen Peroxide 122-130 BCL2, apoptosis regulator Rattus norvegicus 94-99 20933054-6 2011 These results indicate that activation of the intrinsic/mitochondrial apoptosis pathway is essential for cytokine-induced beta cell death and the mitochondrial generation of reactive oxygen species, in particular mitochondrial hydrogen peroxide, differentially regulates the Bax/Bcl-2 ratio. Hydrogen Peroxide 227-244 BCL2, apoptosis regulator Rattus norvegicus 279-284 20804591-7 2010 Furthermore, H2O2 treatment also caused a marked reduction in the expression of Bcl-2 while no significant change of Bax was observed. Hydrogen Peroxide 13-17 BCL2, apoptosis regulator Rattus norvegicus 80-85 20629637-4 2010 Results indicated that the MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] inhibitor (PD98059) and 10 muM Sal B remarkably prevented BMSCs from H2O2-induced apoptosis through attenuating caspase-3 activation, which is accompanied by the significant up-regulation of Bcl-2. Hydrogen Peroxide 193-197 BCL2, apoptosis regulator Rattus norvegicus 315-320 20813162-4 2010 We demonstrated that H(2)O(2) induces apoptosis in SCs, and is associated with increased release of cytochrome c from mitochondria and the activation of caspase-3 and -9 by up-regulation of Bax and down-regulation of Bcl-2. Hydrogen Peroxide 21-29 BCL2, apoptosis regulator Rattus norvegicus 217-222 21137369-10 2010 Moreover,as detected by Western blot analysis, H2O2 down-regulated the expression of Bcl-2 and up-regulation the expression of Bax compared to control. Hydrogen Peroxide 47-51 BCL2, apoptosis regulator Rattus norvegicus 85-90 19362115-2 2009 Western blot analysis showed that H2O2 increased expression of cleaved form of caspase-3 and proapoptotic Bax protein, but decreased antiapoptotic Bcl-2 protein in H9c2 cell. Hydrogen Peroxide 34-38 BCL2, apoptosis regulator Rattus norvegicus 147-152 19703415-0 2009 Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation. Hydrogen Peroxide 26-43 BCL2, apoptosis regulator Rattus norvegicus 104-109 19703415-3 2009 Here, we report that propofol protects cardiac H9c2 cells from hydrogen peroxide (H(2)O(2))-induced injury by triggering the activation of Akt and a parallel up-regulation of Bcl-2. Hydrogen Peroxide 63-80 BCL2, apoptosis regulator Rattus norvegicus 175-180 19703415-6 2009 The protective effect of propofol on H(2)O(2)-induced injury is reversed by PI3K inhibitor wortmannin, which effectively suppresses propofol-induced activation of Akt, up-regulation of Bcl-2, and protection from apoptosis. Hydrogen Peroxide 37-45 BCL2, apoptosis regulator Rattus norvegicus 185-190 19424680-7 2009 The results showed that exposure of the cells to H(2)O(2) significantly decreased the cell viability, SOD and GSH-Px activities and Bcl-2 expression, and increased LDH release, superoxide anion and MDA generations, caspase 3 activity and Bax expressions. Hydrogen Peroxide 49-57 BCL2, apoptosis regulator Rattus norvegicus 132-137 19731100-3 2010 Exposure of PC12 cells to 0.15 mM H2O2 for 20 min induced a significant decrease in cell viability accompanied by increased oxidative stress, mitochondrial dysfunction, downregulation of Bcl-2, upregulation of Bax, and cell apoptosis. Hydrogen Peroxide 34-38 BCL2, apoptosis regulator Rattus norvegicus 187-192 19657563-7 2009 Western blot analysis demonstrated that the expression of Bcl-2 protein and the activation of pro-caspase-3 were not significantly affected by low dose of H(2)O(2) alone. Hydrogen Peroxide 155-163 BCL2, apoptosis regulator Rattus norvegicus 58-63 17629357-6 2007 LY294002 (a PI3K inhibitor) inhibited the effect of geniposide increasing of Bcl-2 level by activation of MAPK, MEK and c-Raf phosphorylation in hydrogen peroxide treated PC12 cells. Hydrogen Peroxide 145-162 BCL2, apoptosis regulator Rattus norvegicus 77-82 18093848-3 2008 The apoptosis in H2O2-induced PC12 cells was accompanied by downregulation of Bcl-2, upregulation of Bax, the release of mitochondrial cytochrome c into cytosol, and sequential activation of caspase-9 and -3. Hydrogen Peroxide 17-21 BCL2, apoptosis regulator Rattus norvegicus 78-83 18093848-5 2008 Taken together, these results suggest that treatment of PC12 cells with DSS can block H2O2-induced apoptosis by the regulation of Bcl-2 family members, as well as suppression of cytochrome c release and caspase cascade activation. Hydrogen Peroxide 86-90 BCL2, apoptosis regulator Rattus norvegicus 130-135 19148782-7 2009 EGb76 treatment, however, significantly reversed H(2)O(2)-induced reduction of Bcl-2 expression and inhibited Bax expression by 2.3-fold. Hydrogen Peroxide 49-57 BCL2, apoptosis regulator Rattus norvegicus 79-84 19218529-6 2009 The preconditioned cells showed a significant protection against H(2)O(2)-induced loss of cellular viability, membrane damage, and oxygen metabolism accompanied by a significant increase in HIF-1alpha, survivin, phosphorylated Akt (pAkt), and Bcl-2 protein levels and Bcl-2 gene expression. Hydrogen Peroxide 65-73 BCL2, apoptosis regulator Rattus norvegicus 243-248 19218529-6 2009 The preconditioned cells showed a significant protection against H(2)O(2)-induced loss of cellular viability, membrane damage, and oxygen metabolism accompanied by a significant increase in HIF-1alpha, survivin, phosphorylated Akt (pAkt), and Bcl-2 protein levels and Bcl-2 gene expression. Hydrogen Peroxide 65-73 BCL2, apoptosis regulator Rattus norvegicus 268-273 18776992-2 2008 In PC12 cells, H(2)O(2)-induced apoptosis was accompanied by the down-regulation of Bcl-2, the up-regulation of Bax, the release of mitochondrial cytochrome c to cytosol, and the activation of caspase-3, -8 and -9. Hydrogen Peroxide 15-23 BCL2, apoptosis regulator Rattus norvegicus 84-89 18776992-5 2008 Taken together, these results suggest that treatment of PC12 cells with salidroside can block H(2)O(2)-induced apoptosis by regulating Bcl-2 family members and by suppressing cytochrome c release and caspase cascade activation. Hydrogen Peroxide 94-102 BCL2, apoptosis regulator Rattus norvegicus 135-140 18272186-5 2008 Western blot data demonstrated that H(2)O(2) induced cleavage of poly(ADP-ribose)polymerase (PARP), downregulated Bcl-X(L) and Bcl-2 in PC12 cells. Hydrogen Peroxide 36-44 BCL2, apoptosis regulator Rattus norvegicus 127-132 18272186-9 2008 These results suggest that the protective effects of CPF and procyanidin B2 against H(2)O(2)-induced apoptosis involve inhibiting the downregulation of Bcl-X(L) and Bcl-2 expression through blocking the activation of JNK and p38 MAPK. Hydrogen Peroxide 84-92 BCL2, apoptosis regulator Rattus norvegicus 165-170 17997946-9 2007 The expression of Bcl-2 protein was up-regulated and the expression of Bax protein was down-regulated in the Co-SZ-treated group as compared with the H2O2-treated group. Hydrogen Peroxide 150-154 BCL2, apoptosis regulator Rattus norvegicus 18-23 15696927-10 2004 CONCLUSION: Activation of M3 receptor showed protective effect on H2O2-induced apoptosis in cultured rat myocytes and this effect might be related to modulating the expression of some genes including Bcl-2 and Fas as well as the downregulation of [Ca2+]i. Hydrogen Peroxide 66-70 BCL2, apoptosis regulator Rattus norvegicus 200-205 17321170-2 2007 The apoptosis in H2O2-induced PC12 cells was accompanied by a decrease in Bcl-2/Bax protein ratio, release of cytochrome c to cytosol and the activation of caspase-3. Hydrogen Peroxide 17-21 BCL2, apoptosis regulator Rattus norvegicus 74-79 17321170-4 2007 These results indicated that TMP blocked H2O2-induced apoptosis by the regulation of Bcl-2 family members, suppression of cytochrome c release, and caspase cascade activation in PC12 cells. Hydrogen Peroxide 41-45 BCL2, apoptosis regulator Rattus norvegicus 85-90 16129420-0 2005 Protection of oxidative preconditioning against apoptosis induced by H2O2 in PC12 cells: mechanisms via MMP, ROS, and Bcl-2. Hydrogen Peroxide 69-73 BCL2, apoptosis regulator Rattus norvegicus 118-123 16129420-3 2005 These results suggested that the preconditioning with low dose of H2O2 could protect the oxidative stress-induced PC12 cells apoptosis not only by preventing the reduction of MMP and expression of Bcl-2 as well as increase in ROS level, but also through overexpression of Bcl-2. Hydrogen Peroxide 66-70 BCL2, apoptosis regulator Rattus norvegicus 197-202 16129420-3 2005 These results suggested that the preconditioning with low dose of H2O2 could protect the oxidative stress-induced PC12 cells apoptosis not only by preventing the reduction of MMP and expression of Bcl-2 as well as increase in ROS level, but also through overexpression of Bcl-2. Hydrogen Peroxide 66-70 BCL2, apoptosis regulator Rattus norvegicus 272-277 16129420-4 2005 It was indicated that overexpression of Bcl-2 may play a key role in the cytoprotection induced by preconditioning with low dose of H2O2 in PC12 cells. Hydrogen Peroxide 132-136 BCL2, apoptosis regulator Rattus norvegicus 40-45 16157298-8 2005 Incubation with H2O2 for 2-4 h decreased Fas expression and the expression of the Fas-related antiapoptotic proteins FLIP(L) and ARC, and increased the expression of the antiapoptotic proteins bcl-2 and xIAP. Hydrogen Peroxide 16-20 BCL2, apoptosis regulator Rattus norvegicus 193-198 15710238-0 2005 3-nitropropionic acid-induced hydrogen peroxide, mitochondrial DNA damage, and cell death are attenuated by Bcl-2 overexpression in PC12 cells. Hydrogen Peroxide 30-47 BCL2, apoptosis regulator Rattus norvegicus 108-113 15710238-8 2005 Overexpression of Bcl-2 leads to almost threefold higher levels of ATP and also decreased the 3-NPA-mediated induction of hydrogen peroxide by over 50%. Hydrogen Peroxide 122-139 BCL2, apoptosis regulator Rattus norvegicus 18-23 15208316-12 2004 These results suggest that NF-kappaB plays a role in bcl-2-mediated protection against H(2)O(2)-induced apoptosis in PC12 cells through augmentation of antioxidant capacity. Hydrogen Peroxide 87-95 BCL2, apoptosis regulator Rattus norvegicus 53-58 15704586-7 2004 The PI of Bax/Bcl-2 protein in H2O2 group was higher (P < 0.01). Hydrogen Peroxide 31-35 BCL2, apoptosis regulator Rattus norvegicus 14-19 15704586-8 2004 When VSMC(s) were incubated with H2O2 plus Salviae miltiorrhizae, the apoptosis rate greatly declined, and at the same time, the PI of Bax/Bcl-2 protein reduced remarkably compared with H2O2 group (P < 0.05 or P < 0.01). Hydrogen Peroxide 33-37 BCL2, apoptosis regulator Rattus norvegicus 139-144 15704586-9 2004 CONCLUSION: Salviae miltiorrhizae could prevent VSMC(s) from H2O2-induced apoptosis by decreasing the Bax/Bcl-2 protein expression. Hydrogen Peroxide 61-65 BCL2, apoptosis regulator Rattus norvegicus 106-111 12704795-0 2003 Anti-apoptotic defense of bcl-2 gene against hydroperoxide-induced cytotoxicity together with suppressed lipid peroxidation, enhanced ascorbate uptake, and upregulated Bcl-2 protein. Hydrogen Peroxide 45-58 BCL2, apoptosis regulator Rattus norvegicus 26-31 15208316-4 2004 In this work, we have investigated the role of bcl-2 in protecting against oxidative death induced by H(2)O(2) in cultured rat pheochromocytoma PC12 cells. Hydrogen Peroxide 102-110 BCL2, apoptosis regulator Rattus norvegicus 47-52 15037029-2 2004 The apoptosis in H2O2-induced PC12 cells was accompanied by down-regulation of Bcl-2, up-regulation of Bax, the release of mitochondrial cytochrome c to cytosol and sequential activation of caspase-1 and caspase-3 then leading to cleavage of poly-ADP-ribose polymerase (PARP). Hydrogen Peroxide 17-21 BCL2, apoptosis regulator Rattus norvegicus 79-84 15037029-4 2004 Taken together, these results suggest that treatment of PC12 cells with catalpol can block H2O2-induced apoptosis by the regulation of Bcl-2 family members, as well as suppression of cytochrome c release and caspase cascade activation. Hydrogen Peroxide 91-95 BCL2, apoptosis regulator Rattus norvegicus 135-140 12721309-2 2003 Since Bcl-2 family proteins are key regulators of apoptosis, we examined the effects of H2O2 on the expression of principal Bcl-2 family proteins (Bcl-2, Bcl-xL, Bax, Bad) in neonatal rat cardiac myocytes. Hydrogen Peroxide 88-92 BCL2, apoptosis regulator Rattus norvegicus 124-129 12721309-2 2003 Since Bcl-2 family proteins are key regulators of apoptosis, we examined the effects of H2O2 on the expression of principal Bcl-2 family proteins (Bcl-2, Bcl-xL, Bax, Bad) in neonatal rat cardiac myocytes. Hydrogen Peroxide 88-92 BCL2, apoptosis regulator Rattus norvegicus 124-129 12721309-4 2003 Bcl-2, Bax, and Bad were all down-regulated in myocytes exposed to 0.2 mm H2O2, a concentration that induces apoptosis. Hydrogen Peroxide 74-78 BCL2, apoptosis regulator Rattus norvegicus 0-5 14505808-6 2003 Also, it prevented the H(2)O(2)-mediated mitochondrial dysfunction, including disruption of mitochondria membrane permeability transition as well as an increase in expression of apoptogenic Bcl-2 proteins, Bcl-2 and Bcl-X(L). Hydrogen Peroxide 23-31 BCL2, apoptosis regulator Rattus norvegicus 190-195 14505808-6 2003 Also, it prevented the H(2)O(2)-mediated mitochondrial dysfunction, including disruption of mitochondria membrane permeability transition as well as an increase in expression of apoptogenic Bcl-2 proteins, Bcl-2 and Bcl-X(L). Hydrogen Peroxide 23-31 BCL2, apoptosis regulator Rattus norvegicus 206-211 12706234-5 2003 Western blot analysis showed an increase in Bax/Bcl-2 ratio, calpain activity, and caspase-3 activity following treatment with H(2)O(2), and estrogen pretreatment decreased levels of all three. Hydrogen Peroxide 127-135 BCL2, apoptosis regulator Rattus norvegicus 48-53 12704795-0 2003 Anti-apoptotic defense of bcl-2 gene against hydroperoxide-induced cytotoxicity together with suppressed lipid peroxidation, enhanced ascorbate uptake, and upregulated Bcl-2 protein. Hydrogen Peroxide 45-58 BCL2, apoptosis regulator Rattus norvegicus 168-173 12603823-3 2003 Treatment of H19-7 cells with hydrogen peroxide (150 micro m) resulted in a 40% decrease in Bcl-2 protein and a parallel decrease in bcl-2 mRNA levels. Hydrogen Peroxide 30-47 BCL2, apoptosis regulator Rattus norvegicus 92-97 12603823-3 2003 Treatment of H19-7 cells with hydrogen peroxide (150 micro m) resulted in a 40% decrease in Bcl-2 protein and a parallel decrease in bcl-2 mRNA levels. Hydrogen Peroxide 30-47 BCL2, apoptosis regulator Rattus norvegicus 133-138 12697403-0 2003 Hydrogen peroxide-dependent declines in Bcl-2 induces apoptosis in hypoxic liver. Hydrogen Peroxide 0-17 BCL2, apoptosis regulator Rattus norvegicus 40-45 12697403-9 2003 CONCLUSION: Hydrogen peroxide-dependent declines in Bcl-2 induce apoptosis in SECs in the hypoxic rat liver. Hydrogen Peroxide 12-29 BCL2, apoptosis regulator Rattus norvegicus 52-57 10229685-0 1999 Protection against hydrogen peroxide cytotoxicity in rat-1 fibroblasts provided by the oncoprotein Bcl-2: maintenance of calcium homoeostasis is secondary to the effect of Bcl-2 on cellular glutathione. Hydrogen Peroxide 19-36 BCL2, apoptosis regulator Rattus norvegicus 99-104 11045015-8 2000 These results suggest that cytochrome c and caspase-9 initiate the activation of executor caspase-3 in H2O2-treated PC12 cells, and that Bcl-2 inhibits H2O2-induced release of cytochrome c from mitochondria and then proteolytic processing of procaspase-9. Hydrogen Peroxide 103-107 BCL2, apoptosis regulator Rattus norvegicus 137-142 11045015-8 2000 These results suggest that cytochrome c and caspase-9 initiate the activation of executor caspase-3 in H2O2-treated PC12 cells, and that Bcl-2 inhibits H2O2-induced release of cytochrome c from mitochondria and then proteolytic processing of procaspase-9. Hydrogen Peroxide 152-156 BCL2, apoptosis regulator Rattus norvegicus 137-142 11522938-3 2001 RT-PCR studies showed up-regulated p53 and Bax but lowered Bcl-2 mRNA levels with H2O2 treatment. Hydrogen Peroxide 82-86 BCL2, apoptosis regulator Rattus norvegicus 59-64 10229685-2 1999 Studying H2O2-induced cell injury in Rat-1 fibroblast cells, we observed that Bcl-2 had a protective effect against the increase in cytosolic calcium concentration and subsequent cell death. Hydrogen Peroxide 9-13 BCL2, apoptosis regulator Rattus norvegicus 78-83 10229685-3 1999 Furthermore, overexpression of Bcl-2 resulted in an alteration of cellular glutathione status: the total amount of cellular glutathione was increased by about 60% and the redox potential of the cellular glutathione pool was maintained in a more reduced state during H2O2 exposure compared with non-Bcl-2-expressing controls. Hydrogen Peroxide 266-270 BCL2, apoptosis regulator Rattus norvegicus 31-36 9231709-1 1997 Expression of the BCL-2 protein family members, BAX, BAK, BAD, BCL-xL, BCL-xS, and BCL-2, was measured (by western blotting using specific antibodies) in PC12 cells before and during apoptosis induced by either H2O2 treatment or by serum deprivation and during rescue from apoptosis by nerve growth factor (NGF). Hydrogen Peroxide 211-215 BCL2, apoptosis regulator Rattus norvegicus 18-23 9422344-0 1998 Bcl-2 protects isolated plasma and mitochondrial membranes against lipid peroxidation induced by hydrogen peroxide and amyloid beta-peptide. Hydrogen Peroxide 97-114 BCL2, apoptosis regulator Rattus norvegicus 0-5 9422344-10 1998 Collectively, our data suggest that Bcl-2 is localized to mitochondrial and plasma membranes where it can act locally to suppress oxidative damage induced by A beta and H2O2, further highlighting the important role of lipid peroxidation in apoptosis. Hydrogen Peroxide 169-173 BCL2, apoptosis regulator Rattus norvegicus 36-41 9396461-9 1997 Northern blot analysis indicated that bcl-2 and c-fos but not p53 and c-myc may participate in mediating H2O2-Fe(II)-induced VSMC apoptosis. Hydrogen Peroxide 105-109 BCL2, apoptosis regulator Rattus norvegicus 38-43 10229685-6 1999 We therefore suggest that the protection exerted by Bcl-2 against H2O2-induced cytosolic calcium elevation and subsequent cell death is secondary to its effect on the cellular glutathione metabolism. Hydrogen Peroxide 66-70 BCL2, apoptosis regulator Rattus norvegicus 52-57 9890971-3 1999 Bcl-2 expression conferred resistance to apoptosis induced by staurosporine and by oxidative insults including hydrogen peroxide and peroxynitrite, but was less effective in inhibition of activation-induced programmed cell death induced by concanavalin A. Concanavalin A-induced apoptosis was abated, however, in cells expressing very high levels of bcl-2. Hydrogen Peroxide 111-128 BCL2, apoptosis regulator Rattus norvegicus 0-5 9730968-5 1998 NRK cells transfected with Bcl-2 (NRK-Bcl-2) were significantly more resistant to H2O2-induced cytotoxicity than control cells. Hydrogen Peroxide 82-86 BCL2, apoptosis regulator Rattus norvegicus 27-32 9730968-5 1998 NRK cells transfected with Bcl-2 (NRK-Bcl-2) were significantly more resistant to H2O2-induced cytotoxicity than control cells. Hydrogen Peroxide 82-86 BCL2, apoptosis regulator Rattus norvegicus 34-43 9730968-7 1998 Compared with controls, cells overexpressing Bcl-2 showed a delayed rise in intracellular Ca2+ concentration ([Ca2+]i) after H2O2 treatment. Hydrogen Peroxide 125-129 BCL2, apoptosis regulator Rattus norvegicus 45-50 9231709-8 1997 The similarity between changes in expression of BCL-2-related proteins induced by H2O2 exposure and NGF rescue could reflect activation in part of a common antioxidant pathway. Hydrogen Peroxide 82-86 BCL2, apoptosis regulator Rattus norvegicus 48-53 34887995-5 2021 In the further exploration, the Bcl-2 expression was decreased by the p53 overexpression and increased by p53 knockdown in H2O2-treated H9C2 cells. Hydrogen Peroxide 123-127 BCL2, apoptosis regulator Rattus norvegicus 32-37 33815102-16 2021 Finally, BCA reversed OVX- or H2O2-induced increases in Bax and Caspase-3 and decreases in Bcl-2 in the hippocampus and primary cultures of hippocampal neurons. Hydrogen Peroxide 30-34 BCL2, apoptosis regulator Rattus norvegicus 91-96 8902618-0 1996 Free radical-independent protection by nerve growth factor and Bcl-2 of PC12 cells from hydrogen peroxide-triggered apoptosis. Hydrogen Peroxide 88-105 BCL2, apoptosis regulator Rattus norvegicus 63-68 8902618-4 1996 Nerve growth factor (NGF) and Bcl-2 inhibited the hydrogen peroxide-induced apoptosis of PC12 cells. Hydrogen Peroxide 50-67 BCL2, apoptosis regulator Rattus norvegicus 30-35 8902618-6 1996 These data suggest that NGF or Bcl-2 protects PC12 cells from hydrogen peroxide-triggered apoptosis independently from ROS production. Hydrogen Peroxide 62-79 BCL2, apoptosis regulator Rattus norvegicus 31-36 34121490-7 2021 In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H2O2-induced PC12 cells. Hydrogen Peroxide 155-159 BCL2, apoptosis regulator Rattus norvegicus 146-151 34121490-8 2021 However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Hydrogen Peroxide 39-43 BCL2, apoptosis regulator Rattus norvegicus 196-201 34887995-3 2021 The results showed that salidroside significantly alleviated cell growth inhibition induced by H2O2 treatment in H9C2 cells, decreased the levels of intracellular ROS and malondialdehyde (MDA), and increased the activity of superoxide dismutase (SOD) and catalase (CAT); meanwhile, salidroside upregulated the expression of Bcl-2 while downregulated the expression of Bax, p53, and caspase-3 in H2O2-treated H9C2 cells. Hydrogen Peroxide 95-99 BCL2, apoptosis regulator Rattus norvegicus 324-329 34216727-12 2021 H2O2 stimulated the activation of Nrf2 and JNK signaling pathways, but TGD increased the extent of Nrf2 antioxidant activation, decreased the activation of JNK, and eventually reversed the H2O2-induced protein expression of p-MKK7, Keap1, HO-1, Cleaved Caspase3 (CL-Casp3), Cleaved Caspase9 (CL-Casp9), Bax, and Bcl-2. Hydrogen Peroxide 189-193 BCL2, apoptosis regulator Rattus norvegicus 312-317 34336035-11 2021 Knockdown of Ephx2 reduced the expressions of Fas, Fasl, Bax, and cleavedcaspase-3 and elevated the expression of Bcl-2 in H2O2-treated IEC-6 cells. Hydrogen Peroxide 123-127 BCL2, apoptosis regulator Rattus norvegicus 114-119 34257805-7 2021 Furthermore, the results of western blotting showed that compared with the control group, the expression of p-PI3K, p-Akt, and Bcl-2 was significantly decreased, while the expression of Caspase-3 and Bax was significantly increased in the H2O2 group. Hydrogen Peroxide 239-243 BCL2, apoptosis regulator Rattus norvegicus 127-132 34257805-8 2021 In the AEE group, AEE pretreatment could upregulate the expression of p-PI3K, p-Akt, and Bcl-2 and downregulate the expression of Caspase-3 and Bax in PC12 cells stimulated with H2O2. Hydrogen Peroxide 178-182 BCL2, apoptosis regulator Rattus norvegicus 89-94 34694244-6 2022 In addition, treatment with GLP-1(9-36) suppressed H2O2-induced apoptosis by attenuating caspase-3 activity and upregulating proapoptotic proteins, Bcl-2 and Bcl-xL. Hydrogen Peroxide 51-55 BCL2, apoptosis regulator Rattus norvegicus 148-153 35496304-10 2022 H2O2 treatment increased the Bax/Bcl2 ratio and cleaved caspase-3 in NRK52E cells, which was counteracted by MAPK inhibitors. Hydrogen Peroxide 0-4 BCL2, apoptosis regulator Rattus norvegicus 33-37 35126791-7 2022 The protein levels of SOD1, SOD2, Bcl-2, and IkappaB-alpha in the H2O2 treatment group were significantly decreased compared with the H2O2+escin group, and the Bax, TNF-alpha, IL-1beta, p65, and IkappaKalpha protein expressions were greatly higher than those in the H2O2+escin group. Hydrogen Peroxide 66-70 BCL2, apoptosis regulator Rattus norvegicus 34-39 33734020-7 2021 MR enhanced the activity of the antioxidant enzyme superoxide dismutase (SOD) and suppressed H2O2-induced downregulation of the antiapoptotic protein Bcl-2 and activation of the proapoptotic protein caspase-3. Hydrogen Peroxide 93-97 BCL2, apoptosis regulator Rattus norvegicus 150-155 33986693-7 2021 On the other hand, H2O2 treatment suppressed the level of antiapoptotic protein Bcl-2, which was further decreased by Panx1 overexpression or mitigated by Panx1 depletion. Hydrogen Peroxide 19-23 BCL2, apoptosis regulator Rattus norvegicus 80-85 33628378-14 2021 Reduced cell proliferation and decreased Bcl-2/Bax ratio induced by H2O2 were rescued by SAB. Hydrogen Peroxide 68-72 BCL2, apoptosis regulator Rattus norvegicus 41-46 33294293-4 2020 By establishing the H2O2-induced injury model, miR-135a-5p transfection was found to inhibit the apoptosis of PC12 cells by downregulating the SP1 gene, which subsequently induced downregulation of pro-apoptotic proteins (Bax, cleaved caspase-3) and upregulation of anti-apoptotic protein Bcl-2. Hydrogen Peroxide 20-24 BCL2, apoptosis regulator Rattus norvegicus 289-294 33075003-8 2020 In addition, the expression of Bcl-2 was significantly reduced, and the expression of Bax and caspase-3 were significantly increased by H2O2 treatment. Hydrogen Peroxide 136-140 BCL2, apoptosis regulator Rattus norvegicus 31-36 32139897-5 2020 The protective effect of hypotonic challenge against H2O2-induced apoptosis was mediated through inhibiting mitochondria-dependent apoptotic pathway, evidenced by increased Bcl-2/Bax ratio, stabilizing mitochondrial membrane potential (MMP), decreased cytochrome c release from the mitochondria to the cytoplasm, and inhibition of the activation of caspase-9 and caspase-3. Hydrogen Peroxide 53-57 BCL2, apoptosis regulator Rattus norvegicus 173-178 30896796-10 2019 The expression of heat shock protein 60 (HSP60), a direct target of miR-1, was identified to be decreased in MI and H2O2-induced apoptosis, which was associated with a decrease in Bcl-2 and an increase in Bax; expression was restored following treatment with carvedilol. Hydrogen Peroxide 116-120 BCL2, apoptosis regulator Rattus norvegicus 180-185 32635976-4 2020 The results showed that the proliferation of H9c2 cells could be inhibited after being treated with 200 muM H2O2 for 12 h, and 100 mug/ml FGF1 could increase the proliferation rate of H9c2 cells, mitochondrial membrane potential and the mRNA expression of Bcl-2, and reduce the ROS accumulation, the level of apoptosis, the content of intracellular calcium and the mRNA expression of Bax and Caspase-3 caused by H2O2. Hydrogen Peroxide 108-112 BCL2, apoptosis regulator Rattus norvegicus 256-261 30058479-9 2020 Real-time PCR of PC12 cells showed that 150 microM H2O2 treatment increased the ratio of Bax/Bcl-2 while vitamin K2 (20 and 50 muM) reduced the rate. Hydrogen Peroxide 51-55 BCL2, apoptosis regulator Rattus norvegicus 93-98 32382683-6 2020 We discovered that edaravone attenuated H2O2-induced oxidative stress by reactivating the Akt signaling axis and antagonistically restoring the expression of apoptosis associated regulators such as Bcl-2 and Caspase-3. Hydrogen Peroxide 40-44 BCL2, apoptosis regulator Rattus norvegicus 198-203 31326407-12 2019 Hyperoside treatment caused a decrease in Bax expression and an increase in Bcl-2 expression in H2O2-stimulated granulosa cells. Hydrogen Peroxide 96-100 BCL2, apoptosis regulator Rattus norvegicus 76-81 32580730-11 2020 Meanwhile, IkappaBalpha overexpression decreased H2O2-induced apoptosis by upregulating the Bcl-2/Bax ratio and reduced autophagy by downregulating the expression of Beclin-1 and the LC3-II/LC3-I ratio. Hydrogen Peroxide 49-53 BCL2, apoptosis regulator Rattus norvegicus 92-97 32542430-8 2020 It was also evidenced that upon restoring the levels of Bcl-2 with the help of pc-DNA3-Bcl-2 halted the attenuating action of miR-466c-3p in hydrogen peroxide exposed N9 microglia cells. Hydrogen Peroxide 141-158 BCL2, apoptosis regulator Rattus norvegicus 56-61 32542430-8 2020 It was also evidenced that upon restoring the levels of Bcl-2 with the help of pc-DNA3-Bcl-2 halted the attenuating action of miR-466c-3p in hydrogen peroxide exposed N9 microglia cells. Hydrogen Peroxide 141-158 BCL2, apoptosis regulator Rattus norvegicus 87-92 32132961-7 2019 Besides lower expression of Bax-1 and lower content of malondialdehyde (MDA) were detected after H2O2 treatment, we also found higher expression of Bcl-2 in Keap1 ATG codon knock-out cells, whereas a higher expression of PCNA was observed only in the Keap1 376th codon-edited cells, whose Bax-1 expression was lower than that in the control cells. Hydrogen Peroxide 97-101 BCL2, apoptosis regulator Rattus norvegicus 148-153 31207343-8 2019 Furthermore, AE treatment significantly reversed H2O2-induced upregulation of Bax/Bcl-2 and the loss of mitochondrial membrane potential. Hydrogen Peroxide 49-53 BCL2, apoptosis regulator Rattus norvegicus 82-87 30896883-0 2019 Activation of the ERK/Creb/Bcl-2 pathway protects periodontal ligament stem cells against hydrogen peroxide-induced oxidative stress. Hydrogen Peroxide 90-107 BCL2, apoptosis regulator Rattus norvegicus 27-32 30984338-5 2019 Furthermore, we revealed that H2-O2 mixture blocked c-Jun N-terminal kinase- (JNK-) MAPK activation, increased the ratio of Bcl-2/Bax, and inhibited caspase 3 cleavage to protect against CIH-induced cardiac apoptosis. Hydrogen Peroxide 30-35 BCL2, apoptosis regulator Rattus norvegicus 124-129 30876692-4 2019 As a result, CaMEK attenuated H2O2-induced apoptosis and cytotoxicity in NCMs, evidenced by decreased apoptotic cells and the ratio of Bax/Bcl-2, increased the mitochondrial membrane potential (Deltapsim) and cell vitality and reduced the level of lactate dehydrogenase (LDH). Hydrogen Peroxide 30-34 BCL2, apoptosis regulator Rattus norvegicus 139-144 30746596-5 2019 EG pretreatment attenuated H2O2-induced mitochondrial dysfunction as indicated by the decreased caspase-9/-3 activation, PARP cleavage, mitochondrial membrane potential (MMP) depletion, Bax/Bcl-2 ratio, cytochrome c release and ROS overproduction. Hydrogen Peroxide 27-31 BCL2, apoptosis regulator Rattus norvegicus 190-195 30529124-6 2019 AFWE obviously reversed the alternations as H2O2 increased Caspase-3 and decreased the ratio of Bcl-2/Bax expressions. Hydrogen Peroxide 44-48 BCL2, apoptosis regulator Rattus norvegicus 96-101 30529106-9 2019 Compared with the NC group, the MnSOD overexpression group treated with different concentrations of Res (0, 25, 50, 100, or 200 muM) and 5 muM H2O2 showed reduced levels of mitochondrial reactive oxygen species, increased B-cell-lymphoma-2 (Bcl-2), reduced Bcl-2 Associated X protein (Bax), and fewer apoptotic cells. Hydrogen Peroxide 143-147 BCL2, apoptosis regulator Rattus norvegicus 222-239 30529106-9 2019 Compared with the NC group, the MnSOD overexpression group treated with different concentrations of Res (0, 25, 50, 100, or 200 muM) and 5 muM H2O2 showed reduced levels of mitochondrial reactive oxygen species, increased B-cell-lymphoma-2 (Bcl-2), reduced Bcl-2 Associated X protein (Bax), and fewer apoptotic cells. Hydrogen Peroxide 143-147 BCL2, apoptosis regulator Rattus norvegicus 241-246 30059683-5 2018 Exposure of PC12 cells to 150 muM H2O2 or 20 muM Abeta1-42 down-regulated anti-apoptotic protein expression (Bcl-2), up-regulated pro-apoptotic protein expression (Bax, cytochrome C, and cleaved caspase-3), increased JNK and p38 MAPK phosphorylation and finally caused significant cell death. Hydrogen Peroxide 34-38 BCL2, apoptosis regulator Rattus norvegicus 109-114 30994729-7 2019 An increased Bcl-2 to Bax ratio was also seen in myocytes treated with H2S after H2O2-induced stress. Hydrogen Peroxide 81-85 BCL2, apoptosis regulator Rattus norvegicus 13-18 30651848-10 2019 In addition, the expression of Bcl-2 was significantly reduced and the expression of Bax and caspase-3 were significantly increased by H2O2 treatment. Hydrogen Peroxide 135-139 BCL2, apoptosis regulator Rattus norvegicus 31-36 30662323-11 2019 The suppression of apoptosis by baicalein in H2O2-stimulated cells was associated with reduction of increased Bax/Bcl-2 ratio, activation of caspase-9 and -3, and degradation of poly (ADP-ribose) polymerase. Hydrogen Peroxide 45-49 BCL2, apoptosis regulator Rattus norvegicus 114-119 30276139-0 2018 Effect of Ghrelin on Caspase 3 and Bcl2 Gene Expression in H2O2 Treated Rat"s Bone Marrow Stromal Cells. Hydrogen Peroxide 59-63 BCL2, apoptosis regulator Rattus norvegicus 35-39 29968377-5 2018 KEY RESULTS: Hydrogen peroxide (H2 O2 ) induced BASMC apoptosis through a mitochondria-dependent pathway, including by increasing the apoptosis rate, down-regulating the ratio of Bcl-2/Bax and potentiating the loss of the mitochondrial membrane potential and release of cytochrome c from the mitochondria to the cytoplasm. Hydrogen Peroxide 13-30 BCL2, apoptosis regulator Rattus norvegicus 179-184 29968377-5 2018 KEY RESULTS: Hydrogen peroxide (H2 O2 ) induced BASMC apoptosis through a mitochondria-dependent pathway, including by increasing the apoptosis rate, down-regulating the ratio of Bcl-2/Bax and potentiating the loss of the mitochondrial membrane potential and release of cytochrome c from the mitochondria to the cytoplasm. Hydrogen Peroxide 32-37 BCL2, apoptosis regulator Rattus norvegicus 179-184 29521449-5 2018 The mRNA levels of Bax, Caspase-9, and Caspase-3 were decreased, while the Bcl-2 mRNA level was increased in H2 O2 -induced BRL-3A cells treated with DHEA. Hydrogen Peroxide 109-114 BCL2, apoptosis regulator Rattus norvegicus 75-80 29797135-3 2018 Preincubation with insulin in concentrations of 100 nM and 1 muM significantly increased Bcl-2 content in neurons in 5, 30, and 45 min and 1, 2, and 4 h after the start of cell exposure to H2O2. Hydrogen Peroxide 189-193 BCL2, apoptosis regulator Rattus norvegicus 89-94 29488607-6 2018 Western blot analysis and a caspase-3 substrate assay demonstrated that upregulation of miRNA-23a expression suppressed the Bcl-2-associated X (Bax)/Bcl-2 protein expression ratio, caspase-3 activity level and tumor suppressor p53 (p53) protein expression in H2O2-induced H9C2 cells. Hydrogen Peroxide 259-263 BCL2, apoptosis regulator Rattus norvegicus 124-129 28824312-7 2017 Furthermore, Western blot analysis revealed that OGE pretreatment inhibited H2O2-induced apoptotic protein caspase-3 activation and PARP cleavage, as well as it reversed Bax up-regulation and Bcl-2 down-regulation. Hydrogen Peroxide 76-80 BCL2, apoptosis regulator Rattus norvegicus 192-197 29039516-6 2017 Furthermore, western blotting analysis demonstrated that baicalin markedly attenuated H2O2-induced cell apoptosis, as demonstrated by the down-regulation of cleaved caspase-3 and the increase in the apoptosis regulator Bcl-2 (Bcl-2)/apoptosis regulator BAX (Bax) ratio following baicalin treatment in H2O2-treated H9c2 cells. Hydrogen Peroxide 86-90 BCL2, apoptosis regulator Rattus norvegicus 219-224 29039516-6 2017 Furthermore, western blotting analysis demonstrated that baicalin markedly attenuated H2O2-induced cell apoptosis, as demonstrated by the down-regulation of cleaved caspase-3 and the increase in the apoptosis regulator Bcl-2 (Bcl-2)/apoptosis regulator BAX (Bax) ratio following baicalin treatment in H2O2-treated H9c2 cells. Hydrogen Peroxide 86-90 BCL2, apoptosis regulator Rattus norvegicus 226-231 28962124-11 2017 It was also observed that H2O2 exposure significantly decreased Bcl-2 and mitochondrial Cyt C, while it increased Bax and cleaved-caspase-3, which were attenuated by allicin pretreatment. Hydrogen Peroxide 26-30 BCL2, apoptosis regulator Rattus norvegicus 64-69 29931925-10 2017 CONCLUSIONS: bFGF could attenuate oxidative injury of rat myoblasts induced by hydrogen peroxide, which mechanism might be related to enhanced Bcl-2 and reduced ROS, Cyt. Hydrogen Peroxide 79-96 BCL2, apoptosis regulator Rattus norvegicus 143-148 28176145-6 2017 Propofol significantly suppressed the H2O2-induced elevations in the activities of caspases 3, 8, 9 and 12, the ratio of Bax/Bcl-2, and cell apoptosis. Hydrogen Peroxide 38-42 BCL2, apoptosis regulator Rattus norvegicus 125-130 28378219-5 2017 However, KR-33889 pretreatment significantly attenuated H2O2-induced apoptosis of H9c2 cells, which was accompanied by decrease in expression of both cleaved caspase-3 and Bax and increase in Bcl-2 expression and the ratio of Bcl-2/Bax. Hydrogen Peroxide 56-60 BCL2, apoptosis regulator Rattus norvegicus 192-197 28378219-5 2017 However, KR-33889 pretreatment significantly attenuated H2O2-induced apoptosis of H9c2 cells, which was accompanied by decrease in expression of both cleaved caspase-3 and Bax and increase in Bcl-2 expression and the ratio of Bcl-2/Bax. Hydrogen Peroxide 56-60 BCL2, apoptosis regulator Rattus norvegicus 226-231 28439402-5 2017 Curcumin also decreased the cleaved caspase-3 (CC3) protein expression level and increased the Bcl-2/Bax ratio in H2O2-stimulated H9c2 cells. Hydrogen Peroxide 114-118 BCL2, apoptosis regulator Rattus norvegicus 95-100 28135600-4 2017 Furthermore, H2O2 treatment significantly upregulated the protein expression of Bax, cleaved caspases 3 and cytosolic cytochrome c, and down-regulated Bcl-2 levels. Hydrogen Peroxide 13-17 BCL2, apoptosis regulator Rattus norvegicus 151-156 28281874-5 2017 Both XN extracts effectively protected PC12 cells against H2O2-induced cell damage by inhibiting release of lactate dehydrogenase, decreasing DNA damage, restoring mitochondrial membrane potential, and arresting abnormal apoptosis through upregulation of Bcl-2 and downregulation of Bax and caspase 3. Hydrogen Peroxide 58-62 BCL2, apoptosis regulator Rattus norvegicus 255-260 28123342-8 2017 Overexpression of miR-135a blocked the Bcl-2 protein and enhanced the apoptosis induced by H2O2, and miR-135a inhibition restored Bcl-2 protein expression. Hydrogen Peroxide 91-95 BCL2, apoptosis regulator Rattus norvegicus 39-44 27817140-7 2017 The 20 microM of H2O2 treatment induced OS by elevating total ROS level, reduced catalase and Bcl-2 expression levels with overexpression of Bax and cytochrome c and induced DNA fragmentation in denuded eggs cultured in vitro. Hydrogen Peroxide 17-21 BCL2, apoptosis regulator Rattus norvegicus 94-99 27401065-9 2017 Jatrorrhizine also attenuated the H2O2-induced Bcl-2/Bax ratio reduction and caspase-3 activation in these neurons. Hydrogen Peroxide 34-38 BCL2, apoptosis regulator Rattus norvegicus 47-52 28123342-8 2017 Overexpression of miR-135a blocked the Bcl-2 protein and enhanced the apoptosis induced by H2O2, and miR-135a inhibition restored Bcl-2 protein expression. Hydrogen Peroxide 91-95 BCL2, apoptosis regulator Rattus norvegicus 130-135 28123342-10 2017 The results of the present study indicate that miR-135a regulates H2O2-induced apoptosis in H9c2 cells via targeting Bcl-2, and that miR-135a may be a novel therapeutic target for ischemic heart disease. Hydrogen Peroxide 66-70 BCL2, apoptosis regulator Rattus norvegicus 117-122 27593219-10 2016 Moreover, exposure to H2O2 significantly increased the levels of Bax, p53, cleaved caspase-8, and cleaved caspase-9, and decreased the level of Bcl-2, resulting in cell apoptosis. Hydrogen Peroxide 22-26 BCL2, apoptosis regulator Rattus norvegicus 144-149 26854628-9 2016 In addition, EndoII siRNA aggravated, but EndoII overexpression alleviated, the reduction of Bcl-2 expression in H2O2-treated cells. Hydrogen Peroxide 113-117 BCL2, apoptosis regulator Rattus norvegicus 93-98 27446335-9 2016 Western blot analysis demonstrated that H2O2-induced reductions in B cell lymphoma 2 (Bcl-2) expression levels were reversed by tanshinone IIA. Hydrogen Peroxide 40-44 BCL2, apoptosis regulator Rattus norvegicus 67-84 27446335-9 2016 Western blot analysis demonstrated that H2O2-induced reductions in B cell lymphoma 2 (Bcl-2) expression levels were reversed by tanshinone IIA. Hydrogen Peroxide 40-44 BCL2, apoptosis regulator Rattus norvegicus 86-91 27446335-10 2016 In addition, the effect of tanshinone IIA on Bcl-2 protein expression level in an oxidative environment was suppressed by a PI3K inhibitor, wortmannin, indicating that tanshinone IIA exerts cardioprotective effects against H2O2-induced cell death via the activation of the PI3K/Akt signal transduction pathway and the consequent upregulation of Bcl-2. Hydrogen Peroxide 223-227 BCL2, apoptosis regulator Rattus norvegicus 45-50 27166426-7 2016 We observed that apoptosis in H9c2 was associated with increased Bax, cytochrome c, caspase-3, decreased Bcl-2 activity after 24 h of H2O2 exposure. Hydrogen Peroxide 134-138 BCL2, apoptosis regulator Rattus norvegicus 105-110 27430346-9 2016 In addition, cannabidiol reduced caspase-3 gene expression and augmented the Bcl-2 protein expression levels in the nucleus pulposus cells following H2O2 exposure. Hydrogen Peroxide 149-153 BCL2, apoptosis regulator Rattus norvegicus 77-82 25955519-5 2015 Furthermore, we found that following exposure to OGD or H2O2, the knockdown of Srxn1 resulted in a decrease in mitochondrial transmembrane potential (Deltapsim) as indicated by JC-1 staining, an increase in the cytoplasmic expression of cytochrome c (Cyt.C), caspase-3, caspase-9, poly(ADP-ribose) polymerase (PARP) and Bax protein at the protein level, but a decrease in the expression of the anti-apoptotic Bcl-2 protein; these effects were tightly associated with the mitochondrial apoptotic pathway. Hydrogen Peroxide 56-60 BCL2, apoptosis regulator Rattus norvegicus 409-414 26282432-11 2015 Furthermore, FrzA over-expression decreased the apoptotic rate, and the Bax/Bcl-2 ratio in cardiomyocytes treated with H2O2. Hydrogen Peroxide 119-123 BCL2, apoptosis regulator Rattus norvegicus 76-81 27096070-8 2016 Western blot data revealed that the inhibitory effect of C4 on H2O2-induced up and down-regulation of Bcl-2, Bax, caspase-3, and cleaved caspase-3. Hydrogen Peroxide 63-67 BCL2, apoptosis regulator Rattus norvegicus 102-107 26414235-7 2016 The data showed that LY294002 almost had the same effects with H(2)O(2), which was also significantly reversed by quercetin could enhance Bax/Bcl-2 ratio and adjust the p-Akt expression, which indicated quercetin might protect PC12 cells against the negative effect of H(2)O(2) via activating the PI3K/Akt signal pathway. Hydrogen Peroxide 63-71 BCL2, apoptosis regulator Rattus norvegicus 142-147 26359087-10 2015 Furthermore, DZ preconditioned DM-EPCs exhibited up-regulated expression of prosurvival genes (VEGF, SDF-1alpha, HGF, bFGF, and Bcl2) on exposure to H2O2, and VEGF and Bcl2 on exposure to hyperglycemia while down regulation of Caspase-3 gene. Hydrogen Peroxide 149-153 BCL2, apoptosis regulator Rattus norvegicus 128-132 26359087-10 2015 Furthermore, DZ preconditioned DM-EPCs exhibited up-regulated expression of prosurvival genes (VEGF, SDF-1alpha, HGF, bFGF, and Bcl2) on exposure to H2O2, and VEGF and Bcl2 on exposure to hyperglycemia while down regulation of Caspase-3 gene. Hydrogen Peroxide 149-153 BCL2, apoptosis regulator Rattus norvegicus 168-172 26073340-7 2015 Pretreatment with YGS40 significantly prevented H2O2-induced cytotoxicity and protected the cells against H2O2-triggered apoptosis characterized by externalization of membrane phosphatidylserine and caspase-3 activation and the increased ratio of Bax/Bcl-2 in PC12 cells. Hydrogen Peroxide 106-110 BCL2, apoptosis regulator Rattus norvegicus 251-256 26136891-5 2015 The H2O2-induced apoptosis of PC12 cells resulted in a reduction in the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein ratio and the activation of caspase-3. Hydrogen Peroxide 4-8 BCL2, apoptosis regulator Rattus norvegicus 72-89 26136891-5 2015 The H2O2-induced apoptosis of PC12 cells resulted in a reduction in the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein ratio and the activation of caspase-3. Hydrogen Peroxide 4-8 BCL2, apoptosis regulator Rattus norvegicus 91-96 26136891-5 2015 The H2O2-induced apoptosis of PC12 cells resulted in a reduction in the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein ratio and the activation of caspase-3. Hydrogen Peroxide 4-8 BCL2, apoptosis regulator Rattus norvegicus 98-103 25344274-5 2015 Increased Bax/Bcl-2 ratio, mitochondrial membrane potential decrease, cytochrome c release, caspase-9/-3 activation, AIF/Endo G translocation were observed in H2O2-treated cells. Hydrogen Peroxide 159-163 BCL2, apoptosis regulator Rattus norvegicus 14-19 25128810-4 2014 While the treatment of H9c2 cardiomyoblast cells with hydrogen peroxide caused a loss of cell viability and an increase in the number of apoptotic cells, hispidin significantly protected the cells against hydrogen peroxide-induced cell death without any cytotoxicity as determined by XTT assay, LDH release assay, Hoechst 33342 assay, and Western blotting of apoptosis proteins such as caspase-3, Bax, and Bcl-2. Hydrogen Peroxide 54-71 BCL2, apoptosis regulator Rattus norvegicus 406-411 25146667-9 2014 Moreover, phillyrin could inhibit H2O2-induced up-regulation of Bax/Bcl-2 ratio. Hydrogen Peroxide 34-38 BCL2, apoptosis regulator Rattus norvegicus 68-73 25174114-6 2014 RESULTS: Compared with normal control group, in the H2O2 group, the production of ROS and the apoptosis rate significantly increased in rNPCs; CGA treatment inhibited ROS production and cell apoptosis, while increased the expression of p-Akt and BCL-2; LY294002, a PI3Kinse inhibitor, not only decreased the expression of p-Akt and BCL-2, but also obviously increased ROS production and cell apoptosis. Hydrogen Peroxide 52-56 BCL2, apoptosis regulator Rattus norvegicus 246-251 24963995-13 2014 In both H2O2-treated BV-2 microglia and glaucoma models, caspase 3, cytochrome c, and BAX were downregulated and BCL2 was upregulated in the curcumin-treated group. Hydrogen Peroxide 8-12 BCL2, apoptosis regulator Rattus norvegicus 113-117 24286466-0 2014 Insulin on hydrogen peroxide-induced oxidative stress involves ROS/Ca2+ and Akt/Bcl-2 signaling pathways. Hydrogen Peroxide 11-28 BCL2, apoptosis regulator Rattus norvegicus 80-85 25174114-6 2014 RESULTS: Compared with normal control group, in the H2O2 group, the production of ROS and the apoptosis rate significantly increased in rNPCs; CGA treatment inhibited ROS production and cell apoptosis, while increased the expression of p-Akt and BCL-2; LY294002, a PI3Kinse inhibitor, not only decreased the expression of p-Akt and BCL-2, but also obviously increased ROS production and cell apoptosis. Hydrogen Peroxide 52-56 BCL2, apoptosis regulator Rattus norvegicus 332-337 25206571-6 2013 Real-time PCR and western blot analysis showed that high and medium doses of 5-hydroxymethylfurfural prevented H2O2-induced up-regulation of p53, Bax and caspase-3 and an-tagonized the down-regulation of Bcl-2 induced by H2O2 treatment. Hydrogen Peroxide 111-115 BCL2, apoptosis regulator Rattus norvegicus 204-209 25015774-11 2014 Overexpression of active MEK5 or KLF4 in H2O2-stressed cells increased Bcl-2/Bax ratio and the expression of NAIP (neuronal apoptosis inhibitory protein). Hydrogen Peroxide 41-45 BCL2, apoptosis regulator Rattus norvegicus 71-76 25404948-0 2014 Protection of Tong-Sai-Mai Decoction against Apoptosis Induced by H2O2 in PC12 Cells: Mechanisms via Bcl-2-Mitochondria-ROS-INOS Pathway. Hydrogen Peroxide 66-70 BCL2, apoptosis regulator Rattus norvegicus 101-106 25404948-7 2014 Our findings revealed that TSM cotreatment with H2O2 restores the expression of bcl-2, inducible nitric oxide synthase (INOS), and mitochondria membrane potential. Hydrogen Peroxide 48-52 BCL2, apoptosis regulator Rattus norvegicus 80-85 24126783-5 2014 Overexpression of IGF-1 prevented MDSCs from H2O2-induced caspase-dependent apoptotic cell death by upregulating the PI3K/AKT pathway, accompanied with an increase of NF-kappaB, p-NF-kappaB, Bcl-2, and VEGF, as well as a decrease of Bax. Hydrogen Peroxide 45-49 BCL2, apoptosis regulator Rattus norvegicus 191-196 24231470-6 2014 The down-regulated Bcl-2 mRNA level and up-regulated Bax, Caspase-9, and Caspase-3 mRNA expression induced by H2O2 or t-BHP could be restored by EPA-enriched PL pretreatment. Hydrogen Peroxide 110-114 BCL2, apoptosis regulator Rattus norvegicus 19-24 25206571-7 2013 These results suggested that 5-hydroxymethylfurfural could inhibit apoptosis of cultured rat hippocampal neurons injured by H2O2 via increase in Bcl-2 levels and decrease in p53, Bax and caspase-3 protein expression levels. Hydrogen Peroxide 124-128 BCL2, apoptosis regulator Rattus norvegicus 145-150 24455422-6 2013 Moreover, CE was found to reverse the hydrogen peroxide-induced downregulation of active AKT and Bcl-2. Hydrogen Peroxide 38-55 BCL2, apoptosis regulator Rattus norvegicus 97-102 23770344-8 2013 Furthermore, ICD inhibited cell apoptosis and Bax/Bcl-2 ratio induced by H2O2. Hydrogen Peroxide 73-77 BCL2, apoptosis regulator Rattus norvegicus 50-55 23977080-8 2013 Furthermore, hydrogen peroxide induced down-regulation of BCL-2 protein and subsequent activation of caspase-3 were inhibited by CPE treatment. Hydrogen Peroxide 13-30 BCL2, apoptosis regulator Rattus norvegicus 58-63 23352507-3 2013 5-AIQ pretreatment significantly protected against H2O2-induced cell death, as determined by the XTT assay, cell counting, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and Western blot analysis of apoptosis-related proteins such as caspase-3, Bax, and Bcl-2. Hydrogen Peroxide 51-55 BCL2, apoptosis regulator Rattus norvegicus 284-289 23212619-13 2013 The results of western blotting showed that alphaB-crystallin overexpression in myocardial cells can reduce the H2O2-induced release of cytochrome c from the mitochondria (P < 0.05), antagonize the H2O2-induced downregulation of Bcl-2 (P < 0.05) and magnify the decrease in phosphorylated AKT levels induced by H2O2 injury (P < 0.05). Hydrogen Peroxide 112-116 BCL2, apoptosis regulator Rattus norvegicus 232-237 23271286-16 2012 SHH/PI3K/Bcl-2 pathway may be implicated in the protection of neurons against H(2)O(2)-induced apoptosis. Hydrogen Peroxide 78-86 BCL2, apoptosis regulator Rattus norvegicus 9-14