缺血预处理加用川芎嗪抑制肠缺血再灌注性肝细胞凋亡

目的研究缺血预处理加川芎嗪抑制肠缺血再灌注大鼠肝细胞凋亡并探讨其可能机制。方法健康SD大鼠50只,随机分为假手术对照(sham,S)组、肠缺血再灌注(intestine ischemical reperfusion,IIR)组、川芎嗪治疗(ligustrazine,LGT)组、缺血预处理(ischemic preconditioning,IPC)组和川芎嗪 缺血预处理(LGT IPC)组5组。用免疫组化法检测肝组织Bcl-2和Bax蛋白表达,用末端脱氧核苷酸转移酶介导的dUTP原位切口末端标记(terminal deoxynucle-otidyltransferase mediated dUTP nick end labeling,TUNEL)技术检测肝细胞凋亡,并测定肝组织超氧化物歧化酶(superoxide dismutase,SOD)和丙二醛(malondialdehyde,MDA)含量。结果LGT IPC组肝细胞凋亡指数明显低于除S组外的其他各组,Bcl-2蛋白表达明显增多,Bax蛋白表达明显减少,Bcl-2/Bax比值增高。同时LGT IPC组肝组织SOD活性增高,MDA含量降低。结论缺血预处理与川芎嗪联合应用对抑制肠缺血再灌注所致的肝细胞凋亡具有显著的协同作用。

Inhibitory effects of ischemic preconditioning plus tetramethylpyrazine on apoptosis of hepatic cell after intestinal ischemia reperfusion in rats

Objective To investigate the effects of ischemic preconditioning(IPC) plus tetramethylpyrazine on apoptosis of hepatic cell in intestinal ischemia reperfusion in rats and explore the possible mechanism.Methods SD rats were randomly divided into sham operated control group(group S),intestinal ischemia reperfusion group(group IIR),tetramethylpyrazine group(group LGT),IPC group(group IPC) and IPC tetramethylpyrazine group(group IPC LGT).Expression of Bcl-2 and Bax protein in liver tissues was detected with immunohistochemistry,and apoptosis of cells in liver tissues was detected with terminal deoxynucleotidyl-transferase mediated dUTP nick end labeling(TUNEL).The activities of superoxide dismutase(SOD) and the content of malondialdehyde(MDA) in liver tissues were determined.Results The apoptosis index of liver cells in group IPC LGT was lower than those in other groups except S group obviously,and the expression of Bcl-2 increased while the expression of Bax decreases which result in the raise of Bcl-2/Bax ratio in this group.At the same time,SOD activity rises up while MDA content declined in liver tissues in group IPC LGT.Conclusion The combined use of tetramethylpyrazine and IPC shows obvious synergistic effects on inhibiting apoptosis in liver tissues after intestinal ischemia reperfusion.