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• W2110963443 abstract "Nitric oxide (NO) attenuates hydrogen peroxide (H2O2)-mediated injury to H9C2 cardiomyoblasts. To examine the role of nitric oxide, cultured H9C2 cardiomyoblasts were treated with H2O2 for 2 h in the presence or absence of the NO donor, diethylamine nitric oxide (DEANO). DEANO (30 μM) attenuated H2O2-induced apoptosis in H9C2 cells. H2O2-exposed H9C2 cells resulted in apoptosis in a time-dependent manner estimated by DNA fragmentation assay, nuclear morphology stained with fluorescent dye, Hoechst 33258 and Annexin V staining. Pretreatment with z-VAD-FMK, a pancaspase inhibitor, or z-DEVD-CHO, a specific caspase-3 inhibitor, completely suppressed the DNA ladder in response to H2O2. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase-1 activity (YVADase) was detected. Treatment of H9C2 cells with 100 μM H2O2, resulted in a strong activation of JNK/SAPK. However, the activation of JNK/SAPK was clearly attenuated by 30 μM DEANO. Furthermore, the dominant negative JNK and SEK1-expressing cells displayed a marked decrease in a number of apoptotic cells. This inhibition of JNK1 in the system is involved in the protection of H2O2-induced apoptosis in H9C2 cardiomyoblasts." @default.
• W2110963443 created "2016-06-24" @default.
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• W2110963443 date "2001-01-01" @default.
• W2110963443 modified "2023-09-27" @default.
• W2110963443 title "SIGNAL TRANSDUCTION OF NITRIC OXIDE DONOR-INDUCED PROTECTION IN HYDROGEN PEROXIDE-MEDIATED APOPTOSIS IN H9C2 CARDIOMYOBLASTS" @default.
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• W2110963443 doi "https://doi.org/10.1081/iph-100103859" @default.
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