中国动脉硬化杂志2011，Vol.19Issue(4)：310-314,5.
硫化氢对氧应激所致心肌细胞损伤的影响及机制
Cardioprotective Mechanism of Hydrogen Sulfide Attenuating Hydrogen Peroxide-induced Rat Neonatal Cardiomyocytes Injury
边云飞 1秦卫伟 1宋晓苏 1肖传实1
作者信息
- 1. 山西医科大学第二医院心内科,山西省太原市,030001
- 折叠
摘要
Abstract
Aim To study the cardioprotective mechanism of hydrogen sulfide (H2S) on oxidative stress induced by hydrogen peroxide. Methods Primary-cultured cardiomyocytes were obtained from neonatal rats, an oxidative stress injury model was established by exposing the cells to H202 for 2 h. To study the cardioprotective mechanism of hydrogen sulfide (H2S) on oxidative stress induced by hydrogen peroxide,the cells were pre-incubated with 1y294002 for 30 min. The morphology change of cardiomyocytes was observed by inverted phase contrast microscope, the activities of lactate dehydrogenase (LDH) and superoxide dismutase (SOD) ,and content malondialdehyde (MDA) were determined, the activation of the PI3K/Akt signal pathway was observed by Western blotting, the cardiomyocytes apoptosis was detected by AnnexinV/PI flow cytometry. Results After exposing to H202 for 2 h, the release of LDH,MDA and apoptosis were increased, the activities of SOD and ratio of Bcl-2/Bad were decreased (P ＜ 0. 05). After pretreated with sodium hydrosulfide (NaHS) for 30 rains, the injury effect was attenuated, moreover, the phosphorylation of Akt, Bad and ratio of Bcl-2/ Bad were upregulated. LY294002 could block the protection effect of NaHs partly. Conclusion H2S can attenuate hydrogen peroxide-induced rat neonatal cardiomyocytes injury, which may involve the PI3K/Akt pathway.关键词
心肌细胞/硫化氢/氧化应激/PI3K/AktKey words
Cardiomyocytes/ Hydrogen Sulfide/ Oxidative Stress/ PI3K/Akt分类
医药卫生引用本文复制引用
边云飞,秦卫伟,宋晓苏,肖传实..硫化氢对氧应激所致心肌细胞损伤的影响及机制[J].中国动脉硬化杂志,2011,19(4):310-314,5.
