摘要
目的探讨人参皂苷Rb1减轻糖尿病大鼠心肌缺血再灌注期间心肌细胞凋亡的机制。方法糖尿病大鼠分为糖尿病缺血再灌注组(模型组)、人参皂苷Rb1组、联合组(人参皂苷Rb1+PI3K抑制剂Wortmaninn组)、Wortmaninn组。模型组结扎左冠状动脉前降支30 min后恢复灌注120 min,人参皂苷Rb1和Wortmaninn分别于缺血前给予。再灌注120 min后,测定心肌梗死区百分比和心肌细胞凋亡百分比,测定心肌磷酸化Akt(p-Akt)表达情况。结果与模型组比较,人参皂苷Rb1组心肌梗死区百分比和心肌细胞凋亡百分比明显减少,而p-Akt表达明显增加;给予PI3K抑制剂Wortmaninn后,联合组与人参皂苷Rb1组相比,心肌梗死区百分比和心肌细胞凋亡百分比明显增加,而p-Akt表达显著降低。结论人参皂苷Rb1减轻糖尿病大鼠心肌缺血再灌注期间心肌细胞凋亡与其激活PI3K/Akt活性有关。
Objective： To investigate the mechanism of ginsenoside Rb1 against myocardial apoptosis during ischemia-reperfusion injury in diabetic rats.Methods： Diabetic rats were divided into 4 groups： the diabetic ischemia group,the ginsenoside Rb1 group,the combination group and the Wortmaninn group.120 minutes recovery after ligation the left anterior descending branch was used in the diabetic ischemia group.Before the ischemia,the ginsenoside Rb1 and Wortmaninn were used in corresponding group.The myocardial infarct size,the percentage of myocardial apoptosis and the p-Akt were detected in these groups.Results： Compared with the diabetic ischemia group,the myocardial size and the percentage of myocardial apoptosis were decreased significantly in the ginsenoside Rb1 group.Meanwhile,the p-Akt expression in this group was increased obviously.After being used the Wortmaninn,the myocardial infarct size and the percentage of myocardial apoptosis were increased remarkably in the combination group.However,the p-Akt expression in this group was decreased significantly.Conclusion： The ginsenoside Rb1 can reduce the diabetic myocardium apoptosis from ischemia-reperfusion injury by activating PI3K/Akt phosphorylation
出处
《中国中医急症》
2012年第7期1080-1081,共2页
Journal of Emergency in Traditional Chinese Medicine
基金
国家自然科学基金课题(30672033)
