摘要目的 观察缺血再灌注(IR)大鼠肾组织凝血纤溶相关物质的蛋白表达并探讨其意义.方法 雄性Wistar大鼠48只被随机分为6组:假手术组(Sham组)、缺血再灌注0、2、6、12、24 h组(IR0h组、IR2h组、IR6h组、IR 12h组、IR 24 h组),每组8只.用无创动脉夹夹闭双肾动脉45 min建立IR模型.HE染色观察肾组织病理改变；免疫组织化学法检测肾组织内皮素(ET-1)、组织型纤溶酶原激活物(tPA)、纤维蛋白原样蛋白2(Fgl-2)凝血酶原酶蛋白的表达.结果 与Sham组相比,IR 24 h组大鼠血BUN及Scr升高,差异有统计学意义(P＜0.05).IR各组肾组织病理改变程度随再灌注时间延长而逐渐加重；与Sham组相比,IR各组肾小管损伤半定量评分明显升高,差异有统计学意义(P＜0.05).IR各组肾ET-1蛋白表达增加,6h达高峰,与Sham组相比差异有统计学意义(P＜0.05).IR各组肾Fgl-2凝血酶原酶表达增加,12h达高峰,24 h基本恢复正常,与Sham组相比,差异有统计学意义(P＜0.05).肾组织t-PA表达增加,12h达高峰,与Sham组相比,差异有统计学意义(P＜0.05).结论 肾脏IR损伤后存在肾组织凝血纤溶相关物质的异常表达,推测后者可能参与了肾脏IR损伤.

abstractsObjective To investigate the expression and significance of related substances of coagulation and fibrinolysis in the rat kidneys with ischemia reperfusion (IR) injury.Methods Forty-eight male Wistar rats were randomly divided into six groups:Sham,IR 0 h,IR 2 h,IR 6 h,IR 12 h and IR 24 h.IR rats were made by occlusion of bilateral renal arteries by bulldog clamp for 45 minutes.Renal pathology was observed by HE staining.The expression of endothelin-1 (ET-1),tissue plasminogen activator (t-PA) and fibrinogen-like protein 2 (Fgl-2) of renal tissue was detected by immunohistochemical method.Results Scr and BUN increased significantly in IR 24 h group compared with sham group(P＜0.05).Renal pathological injury was significantly aggravated with prolonged reperfusion.The semi-quantitative scores of renal tubular injury were increased in all IR group compared with sham group(P＜0.05).The expression of ET-1 was gradually increased before the first six hour after IR and decreased after twelve hour.Compared with sham group,ET-1 was increased significantly in all IR group.The expression of Fgl-2 fibroleukin in renal tissue increased progressively in the first six hour after IR,weaken in IR 12 h group and trended to normal in IR 24 h group.The expression of t-PA increased progressively during the first six hour after IR,maintained this level in IR 12 h group and decreased in IR 24 h group.Conclusion The abnormal expression of related substances of coagulation and fibrinolysis of rats may participate in renal IR injury.