【摘要】 目的观察参附注射液(SFI)对大鼠肠缺血/再灌注损伤(IRI)期间肾组织内血红素加氧酶-1(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)诱导IRI模型。将36只雄性Wistar大鼠随机分为IRI模型组、SFI预处理组和假手术组。SFI预处理组:缺血前30 min静脉恒速泵入SFI 10 ml/kg,阻断SMA造成肠缺血1 h后再开放;IRI模型组:在缺血前30 min用微量泵持续注入等量生理盐水。应用免疫组化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(SCr)、尿素氮(BUN),同时光镜下观察肾组织病理学改变。结果与假手术组比较,IRI模型组HO-1和iNOS表达均显著增强(P均<0.01),SCr、BUN明显增加(P均<0.01);与IRI模型组比较,SFI预处理组HO-1表达明显升高,而iNOS表达及SCr、BUN明显降低(P均<0.05)。病理学检查显示,SFI能明显减轻肠IRI导致的肾组织病理损害。结论SFI能明显减轻肠IRI所致的肾组织损伤,其分子机制为诱导肠IRI后肾组织中HO-1的表达,同时抑制iNOS的表达。更多还原

【Abstract】 Objective To explore the effect of Shen-Fu injection(SFI,参附注射液) on expressions of heme oxygenase-1(HO-1) and inducible nitric oxide synthase(iNOS) in renal failure induced by intestinal ischemia-reperfusion injury(IRI) in rats and its possible mechanism in the protection of kidney.Methods The model of intestinal IRI was induced by clamping superior mesenteric artery(SMA) for 1 hour and then releasing the arterial clamp for 6 hours.Thirty-six male Wistar rats were randomly divided into three groups: IRI model group,SFI pretreatment group and sham operation group.In the SFI pretreatment group,10 ml/kg of SFI was pumped in at constant rate 30 minutes before the ischemia,the SMA was clumped for 1 hour and then released,while in the IRI model group,an equal volume of normal saline was pumped in continuously 30 minutes before the ischemia.The serum creatinine(SCr) and blood urea nitrogen(BUN) were observed respectively.Expressions and distributions of HO-1 and iNOS in the rat kidney tissue were detected by immunohistochemitry and morphometry computer image analysis.The histological changes of kidney were observed under light microscope.Results The expressions of HO-1 and iNOS were markedly higher,and the levels of SCr and BUN were also significantly higher in intestinal IRI model group than those in the sham operation group(all P<0.01).The expression of iNOS and the levels of SCr and BUN were significantly lower,while the expression of HO1 was obviously higher in SFI pretreatment group than those in IRI model group(all P<0.05).Under light microscope,SFI could significantly alleviate the pathologic lesion of kidney caused by intestinal IRI.Conclusion The data suggest that SFI markedly ameliorate renal failure induced by intestinal IRI,and the protective effect of SFI may be related to the inducement of HO1 expression and the inhibition of iNOS expression in kidney tissue after intestinal IRI.更多还原