参附注射液对肠缺血再灌注大鼠肾组织HO-1与iNOS表达的影响

Effect of Shenfu Injection on expression of HO-1 and iNOS in renal failure rats induced by intestinal ischemia-reperfusion

目的:观察参附注射液(SFI)对肠缺血再灌注(IR)大鼠肾组织内血红素加氧酶(HO-1)、诱生型一氧化氮合酶(iNOS)表达的影响,探讨其肾保护作用机制。方法:采用钳闭大鼠肠系膜上动脉(SMA)缺血再灌注模型。健康成年雄性大鼠随机分为缺血再灌注+生理盐水(NS)组(IR+NS)、SFI预处理组(IR+SFI)和假手术组(C)。应用免疫组织化学方法和图像分析系统检测肾组织中HO-1和iNOS的表达和分布,观察各组血清肌酐、尿素氮,同时光镜观察肾脏组织病理形态学改变。结果:与C组比较,IR+NS组HO-1和iNOS表达显著增强(均P<0.01),血清肌酐、尿素氮明显增加(P<0.01);与IR+NS组比较,IR+SFI组HO-1表达明显升高而iNOS表达明显降低(均P<0.05),血清肌酐、尿素氮明显降低。结论:SFI明显减轻肠IR所致的肾组织的损伤,能诱导肠IR后肾组织中HO-1的表达,同时抑制iNOS的表达。

Objective：To explore the effect of Shenfu Injection （SFI） on expression of Heme oxygenase-1 （HO-1） and iNOS （inducible nitric oxide synthase） in renal failure rats induced by intestinal ischemia-reperfusion （IR） and its possible mechanism. Methods：The model of intestinal ischemia-reperfusion was induced by clamping superior mesenteric artery for one hour and then releasing the arterial clamp for six hours. Wistar rats were randomized into three groups：IR＋normal saline group,IR＋SFI group and control group （C group）. The serum creatinine and blood urea nitrogen were observed respectively. Expression of HO-1 and iNOS in rat kidney tissue was detected by immunohistochemitry and morphometry computer image analysis. The histological change of kidney was observed under light microscope. Results：①Compared with C group,expression of HO-1 and iNOS increased markedly in IR＋ normal saline group （P0.01）. The levels of serum creatinine and blood uria nitrogen were significantly upregulated （P0.01）; ②In IR＋SFI group,expression of iNOS was significantly lower than that in IR＋ normal saline group,while expression of HO-1 was obviously higher （P0.05）. The levels of serum creatinine and blood uria nitrogen were signifi cantly decreased. Under light microscope,SFI could signifi cantly alleviate the pathologic lesion of kidney caused by intestinal ischemia-reperfusion. Conclusion：The data suggested that SFI can ameliorate renal failure induced by intestinal ischemia-reperfusion and the protective effect of SFI may be related to the inducement of HO-1 expression and the inhibition of iNOS expression.