中文摘要：

目的：观察淫羊藿苷（ICA）对自发性高血压大鼠（SHR）肾组织病理损伤的影响,并基于核因子κB（NF-κB）信号通路研究其作用机制。方法：将21只SHR随机均分为模型组和ICA低、高剂量组（20、40 mg/kg,记为ICA-L、ICA-H组）,另取7只同源京都大鼠（WKY）为对照组。各组大鼠ig给药,每日2次,连用11周;对照组和模型组大鼠ig等体积双蒸水。观察各组大鼠肾组织病理学变化;蛋白质印迹法检测肾组织磷酸化NF-κB-p65（p-NF-κB-p65）、NF-κB抑制蛋白（IκB）、肿瘤坏死因子α（TNF-α）蛋白的表达。结果：与对照组比较,模型组大鼠肾结构出现紊乱,肾小球囊腔狭窄且不规则;IκB蛋白的表达明显下调,p-NF-κB-p65、TNF-α蛋白的表达均明显上调（P〈0.01）。与模型组比较,ICA-L、ICA-H组大鼠肾组织上述病理变化有所改善;ICA-L、ICA-H组IκB蛋白的表达均明显上调（P〈0.05或P〈0.01）,ICA-H组大鼠p-NF-κB-p65、TNF-α蛋白的表达均明显下调（P〈0.01）,ICA-L组大鼠p-NF-κB-p65蛋白表达明显下调（P〈0.05）,而ICA-L组大鼠TNF-α蛋白表达差异无统计学意义（P〉0.05）。结论：ICA具有改善SHR肾病理性损伤的作用,其机制可能与抑制NF-κB信号通路相关。

英文摘要：

OBJECTIVE：To observe the effect of pathological lesion of renal tissue in rats with spontaneous hypertension（SHR）,and study its mechanisms based on nuclear factor κB（NF-κB）signaling pathway. METHODS：21 SHR were randomly divided into model group and ICA low-dose,high-dose groups（20,40 mg/kg,denoted by ICA-L,ICA-H groups）;other 7 homologous Kyoto rats（WKY）were regarded as control group. All rats were intragastrically administrated,twice a day,for 11 weeks,rats in control group and model group received equal volume of double distilled water,ig. Pathological changes in renal tissue in each group were observed;Western blot method was used to detect protein expressions of p-NF-κB-p65,IκB and TNF-α in renal tissue. RESULTS：Compared with control group,model group showed disorder renal structure,narrow and irregular glomerular cysts;the protein expression of IκB was significantly down-regulated,protein expressions of p-NF-κB-p65 and TNF-α were significantly up-regulated（P〈0.01）. Compared with model group,the above-mentioned changes of rats showed improvement in ICA-L,ICA-H groups;the protein expression of IκB was significantly up-regulated in ICA-L,ICA-H groups（P〈0.05 or P〈0.01）;the protein expressions of p-NF-κB-p65 and TNF-α were significantly down-regulated（P〈0.01）in ICA-H groups;p-NF-κB-p65 protein expression was significantly down-regulated in ICA-L group（P〈0.05）;while there was no significant difference in TNF-α protein expression in ICA-L group（P〉0.05）. CONCLUSIONS：ICA plays a role in improving renal pathological lesion in SHR,and the mechanism may be related to inhibiting NF-κB signaling pathway.