波生坦改善内皮素诱导的心肌细胞损伤

Bosentan reduce the myocardial cell injury induced by endothelin

目的:体外探讨内皮素及一氧化氮(NO)在急性心肌梗死(AMI)后心肌损伤中发挥的作用及内皮素受体作为心肌梗死治疗靶点的价值。方法:选取AMI患者52例(AMI组),健康体检者32例(正常组),检测血浆内皮素及NO水平。运用不同浓度内皮素及其受体拮抗剂波生坦处理H9C2心肌细胞6 h,考察其对心肌细胞活力及乳酸脱氢酶(LDH)的影响。结果:与正常组相比,AMI组血浆内皮素显著升高(P<0.05),NO水平显著降低(P<0.05);内皮素处理H9C2心肌细胞6 h细胞活性降低(P<0.05),LDH升高(P<0.05);内皮素及波生坦同时处理H9C2心肌细胞6 h,细胞活性升高(P<0.05),LDH降低(P<0.05);TUNEL染色法可见内皮素处理组凋亡细胞增多,波生坦处理后有所改善。结论 :内皮素及NO参与心肌梗死后心肌损伤过程,波生坦可降低内皮素诱导的H9C2心肌细胞损伤。

Objective To investigate the effect of endothelin and nitric oxide on myocardial injury after acute myocardial infarction （AMI） and the value of endothelin receptor antagonism as a therapeutic targetin vitro. Methods 52 patients with AMI and 32 health subjects were included in the research. The plasma levels of en dothelin and nitric oxide were measured by ELISA. H9C2 cellswere treated with different concentrations of en dothelin or bosentan for 6 hours, then cell vitality and LDHwere detected. Results Serum endothelin level was obviously higher and NO level was significantly lowerin AMI patients than the healthy individuals （P 〈 0.05）. After treated with different concentrations of endothelin for 6 hours, cell vitality was decreased and LDH level increased significantly with the increasing concentration of endothelin. Cell vitality improved and LDH level decreased when treated withbosentan withdifferent concentrations. Apoptosis examination （TUNEL） showed increas ing apoptosis ceils and improved after treated with bosentan. Conclusion Endothelin and nitric oxide participate in the progress of myocardial injury after AMI. Bosentan can reduce the H9C2 myocardial cell injury induced by endothelin.