曲美他嗪对心肌缺血时细胞骨架损伤的作用

Effects of trimetazidine on myocytoskeleton in ischemic myocardium

目的 探讨心肌缺血时细胞骨架改变并观察曲美他嗪对心肌缺血时细胞骨架损伤的影响 ,为临床应用提供理论依据。方法 将大白鼠随机分为对照组和用药组并制成缺血模型 ,分别于缺血 30 m in、6 0 min、12 0 min时取心肌组织用免疫组化的方法观察肌动蛋白、波形蛋白、肌球蛋白、结蛋白等心肌细胞骨架蛋白的改变 ,并用计算机图象模拟分析系统计算骨架蛋白量的变化。结果 心肌缺血 30 min即有肌动蛋白、肌球蛋白损伤 ,12 0 min时有结蛋白损伤 (P<0 .0 5 )。曲美他嗪干预后 ,心肌缺血 6 0 min、12 0 min时肌动蛋白、肌球蛋白损伤明显减少 (P<0 .0 5 )。结论 心肌缺血时可以导致细胞骨架损伤 。

Objective To observe the change of the several cytoskeleton proteins in ischemic myocardium of animal model,and the protection of trimetazidine to this damage. Methods 30 Wistar white rats were randomly divided into two groups: control group and trimetazidine group. Ischemia model was made by tie up the left coronary artery,after 30min,60min,120min,the ischemic tissue was taken out for study by using immunohistochemistry. Result Ischemia can induce the disruption of cytoskeleton in myocardium, actin and myosin were damaged in 30 minuses, desmin and vimcntin were a little endurable to anoxia, but damaged after 120 minutes of ischemia. However,trimetazidine group showed less damage in 60 and 120 minutes of ischemia in actin,myosin and desmin than control group(P<0.05).Conclution Ischemia can cause the injury of cytoskeleton in myocardium, which is in response to the irreversible injury to myocardium. trimetazidine can protect the cytoskeleton from being damaged in ischemic myocardium by decreasing the cytoskeleton injury.