摘要
目的研究己酮可可碱对缺血心肌的保护作用,并探讨其可能的机制。方法结扎大鼠左冠状动脉前降支,制备急性心肌梗死模型,观察己酮可可碱对缺血心肌的保护作用。酶联免疫吸附测定法检测血清超氧化物歧化酶(superoxide dismutase,SOD)活力和丙二醛(malondialdehyde,MDA)含量,原位末端标记(terminal-deoxynucleoitidyl transferase mediated nick end labeling,TUNEL)法检测己酮可可碱对心肌缺血大鼠心肌细胞凋亡指数的影响,免疫组化法和Western blot法检测Bcl-2和Bax蛋白表达,激光扫描共聚焦技术检测己酮可可碱对细胞内游离钙离子浓度的改变。结果己酮可可碱100 mg.kg-1组心肌梗死面积缩小,心功能明显改善,血清SOD活力明显升高,MDA水平和心肌细胞凋亡指数降低,Bcl-2表达水平明显增加(P<0.01),Bax表达水平明显降低(P<0.01),对60 mmol.L-1氯化钾诱导的[Ca2+]i升高有明显抑制作用。结论己酮可可碱对大鼠缺血心肌具有保护作用,其机制可能是下调[Ca2+]i、抑制心肌细胞凋亡。
Objective To investigate the protective effect of pentoxifylline against myocardial ischemia and detect its possible mechanisms. Methods The effects of pentoxifylline on myocardial ischemia were observed on a model of acute myocardial infarction by a permanent ligation of left anterior descending coronary artery in rats.MDA content and SOD activity were measured by ELISA method.Myocardium apoptosis was tested by TUNEL.Bcl-2 and Bax protein expression were assayed by immunohistochemical and western blot.Laser scanning confocal microscopy was utilized to assay the effect of pentoxifylline on intracellular calcium concentration（i）. Results Pentoxifylline at 100 mg·kg-1 shrunk infarct size of myocardium,decreased MDA content,increased SOD activity,improved heart function of rats with myocardial ischemia,up-regulated Bcl-2 expression as well（P0.01）,down-regulated Bax expression（P0.01）,and markedly inhibitted i induced by 60 mmol·L-1 KCl（P0.01）. Conclusion Pentoxifylline possesses protective effect on myocardial infarction in rats,the possible mechanisms of which are due to drop of i and cardiomyocyte apoptosis inhibition.
出处
《医药导报》
CAS
2011年第11期1401-1406,共6页
Herald of Medicine
基金
国家自然科学基金资助项目(基金编号:81072640/H3102)
