基于核因子-κB、单核细胞趋化蛋白-1研究益肾宁延缓大鼠肾间质纤维化的作用机制

Study on the mechanism of Yishenning delaying renal interstitial fibrosis in rats by intervening with inflammatory mediators nuclear factors-κ B and monocyte chemotactic protein-1

目的 研究益肾宁颗粒对单侧输尿管结扎大鼠肾脏炎症介质核因子-κB(NF-κB)、单核细胞趋化蛋白-1(MCP-1)表达及其他指标的影响,探究益肾宁延缓肾间质纤维化的作用机制。方法 2月龄SD雄性大鼠40只,随机平均分为模型组、益肾宁组、贝那普利组、益肾宁+贝那普利组,应用单侧输尿管结扎模型,造模结束后1周开始灌胃给药,分别于给药后7、14、21 d留取血、尿、肾脏标本,采用免疫组化方法检测肾组织NF-κB及MCP-1的表达,比较各组大鼠血肌酐、尿素氮、24 h尿蛋白定量的差异。结果 益肾宁组、益肾宁+贝那普利组大鼠肾功能各项指标低于模型组及贝那普利组,差异有统计学意义(P <0.05)。各治疗组NF-κB、MCP-1表达均低于模型组,差异有统计学意义(P <0.05)。益肾宁组、益肾宁+贝那普利组各个时期NF-κB、MCP-1表达量低于贝那普利组,差异有统计学意义(P<0.05)。结论 益肾宁可通过抑制单侧输尿管结扎大鼠炎症介质NF-κB、MCP-1的表达,延缓大鼠肾间质纤维化的进展。

Objective To study the effect of Yishenning Granule on the expression of nuclear factor-κB(NF-κB),monocyte chemoattractant protein-1(MCP-1) and other indexes in kidney of rats with unilateral ureteral ligation,and to explore the mechanism of Yishenning in delaying renal interstitial fibrosis.Methods Forty 2-month-old SD male rats were randomly divided into model group,Yishenning group,benazepril group and Yishenning + benazepril group.The unilateral ureteral ligation model was used,and the drug was given by gavage one week after the establishment of the model.Blood,urine and kidney samples were taken at 7,14 and 21 days after administration,respectively,and the expression of NF-κB and MCP-1 in renal tissue was detected by immunohistochemistry.Results The indexes of renal function in Yishenning group,Yishenning+ benazepril group were lower than those in model group and benazepril group,and the differences were statistically significant(P<0.05).The expressions of NF-κB and MCP-1 in each treatment group were all lower than those in the model group,and the differences were statistically significant(P<0.05).The expressions of NF-κB and MCP-1 in Yishenning group and benazepril group,Yishenning + benazepril group were all lower than those in benazepril group,and the differences were statistically significant(P<0.05).Conclusion Yishenning can delay the progress of renal interstitial fibrosis in rats by inhibiting the expression of inflammatory mediators NF-κB and MCP-1 in rats with unilateral ureteral ligation.