[Protective effects of nitric oxide donor on hydrogen peroxide-induced injury of cardiomyocytes].

To investigate the protective effects of nitric oxide (NO) on cardiomyocytes against hydrogen peroxide (H2O2)-induced injury, cultured neonatal cardiomyocytes were divided into three groups: (1) normal group; (2) H2O2 group: cells were treated with H2O2 (0.1 mmol/L) for 4 h; (3) SNAP+ H2O2 group: cells were pretreated with NO donor S-nitroso-N-acetyl-1,1-penicillamine (SNAP, 0.5 mmol/L) 10 min before H2O2 treatment. Colorimetric assay was used to detect cell viability and lactate dehydrogenase (LDH) activity to evaluate cell injury. Apoptotic rate of cardiomyocytes were determined by flow cytometer. Superoxide dismutase (SOD) activity and malonaldehyde (MDA) content were measured by colorimetric assay to evaluate cell antioxidant ability. Intracellular calcium was tested by laser confocal microscopy. The results showed that after treatment with H2O2, cell viability was significantly reduced to 58.3+/-7.6% compared with normal group (93.1+/-6.2 %). LDH activity and apoptotic rates were 1580.5+/-186.7 U/L and 26.4+/-5.7% respectively, significantly higher than that of normal group (631.4+/-75.6 U/L and 0). SNAP pretreatment markedly improved cell viability to 79.7+/-9.3% and reduced LDH activity and apoptotic rates to 957.8+/-110.9 U/L and 9.1+/-3.3%, respectively. Cells treated with H2O2 had a lower SOD activity of 14.73+/-1.68 NU/ml and a higher MDA content of (15.35+/-3.49) micromol/L compared with normal cells (19.67+/-0.85 NU/ml) and (6.95+/-0.83 micromol/L), respectively. Cells with SNAP pretreatment had a higher SOD activity of 21.36+/-3.11 NU/ml and a lower MDA content of 9.12+/-1.47 micromol/L compared with H2O2 group. Intracellular calcium content was reduced by SNAP administration while enhanced by H2O2. Pretreatment with SNAP could antagonize the effect of H2O2 of accelerating intracellular calcium content. Based on the results observed, it is concluded that NO donor SNAP may protect cardiomyocytes from being injured by H2O2. The underlying mechanisms may include improving cell antioxidant ability and reducing intracellular calcium overload.