摘要
目的探讨丙泊酚对大鼠心肌缺血/再灌注(MI/R)后心肌细胞凋亡的影响及其作用机制。方法选用250-300g雄性SD大鼠,制备大鼠MI/R模型[3],给以45min缺血和2h、4h再灌注。根据实验目的,将45只SD大鼠随机均分为3组(n=15)。假手术组(sham组):在冠状动脉前降支(LAD)下穿线,但不结扎,其余操作与其他各组相同;单纯MI/R组(MI/R组):大鼠接受MI/R处理;丙泊酚组(P组):大鼠接受MI/R处理,在再灌注期间给以0.42mg/(kg.h)丙泊酚。再灌注结束后采用DNA原位末端缺口标记技术(TUNEL)测定心肌细胞凋亡比例,免疫组化法测定心肌细胞内抗凋亡分子Akt、Bcl-2和促凋亡分子p38MAPK的表达。结果与假手术组比较,丙泊酚组MI/R诱导的心肌组织的凋亡明显降低(P<0.05)。免疫组化的结果显示,丙泊酚组肌内Akt和Bcl-2的形成增加,p38MAPK的水平降低(P<0.05)。结论本实验结果提示丙泊酚对MI/R后的心肌组织有显著的保护作用,它的这种作用与其对Akt、Bcl-2和p38MAPK的影响密切相关。
Objective To explore the effect of propofol on myocradial apoptosis induced by myocardial ischemia-reperfusion(MI/R) and its potential mechanism. Methods Forty-five Wistar rats weighing 250 - 300 g were randomly divided into three groups: sham operation group (0.9% NaCl) ;MI/R group; propofol group [intravenous infusion 0.42 mg/(kg·h) during reperfusion]. At the end of reperfusion, the ratio of myocardial apoptosis was analyzed with TUNEL assay, and the expression of pAkt, p38 MAPK and Bcl-2 was detected with immunohistochemical staining. Results Compared with sham operation group, myocardial apoptosis decreased significantly in propofol group. The expression of pro-apoptotic p38 MAPK decreased in propfol group, but the expression of antiapoptotic proteins Akt and Bcl-2 significantly increased in cadiomyocytes. Conclusion These results indicate that propofol is more likely to protect cardiomyocytes from the injury of MI/R-induced apoptosis by increasing production of anti-apoptotic proteins.
出处
《山西医科大学学报》
CAS
2007年第11期965-967,1055,共4页
Journal of Shanxi Medical University
关键词
再灌注损伤
丙泊酚
凋亡
reperfusion injury
propofol
apoptosis