胰激肽原酶对链脲佐菌素诱导的糖尿病肾病大鼠肾纤维化的影响及机制分析  

Effects of Pancreatic Kininogenase on Renal Fibrosis in Rats with Streptozotocin-Induced Diabetic Nephropathy and Its Mechanism

作　　者：赵黎[1] 陈华茜[1] 刘巍[1] 杨涛[1] 张任[1] 曾艳[1] 李正东[1] ZHAO Li;CHEN Huaxi;LIU Wei;YANG Tao;ZHANG Ren;ZENG Yan;LI Zhengdong(Department of Renal Medicine,Dongfeng Geneal Hospital Affiliated to Hubei University of Medicine,Shiyan,Hubei,442006,China)

机构地区：[1]湖北医药学院附属国药东风总医院肾内科,湖北省十堰市442006

出　　处：《医学分子生物学杂志》2021年第6期434-438,共5页Journal of Medical Molecular Biology

基　　金：湖北省卫生厅青年科技人才项目(No.2018CFB354)。

摘　　要：目的探究胰激肽原酶(PK)对链脲佐菌素(STZ)诱导的糖尿病肾病(DN)大鼠肾纤维化的影响及机制。方法将雄性Wistar大鼠随机分为健康对照组(Control)、模型组(Model)、低、高剂量胰激肽原酶组(75、150 U/kg)各15只。测定各组大鼠尾动脉收缩压、生化指标及蛋白表达水平;观察肾组织病理形态改变。结果150 U/kg组大鼠在3、6、9周时的收缩压及干预后的尿素氮(BUN)、肌酐(SCr)、β-2微球蛋白(β2-MG)、Caspase-3、Caspase-9表达水平显著低于Model组和75 U/kg组(P<0.05);一氧化氮(NO)水平显著高于Model组和75 U/kg组(P<0.05)。染色结果显示,PK处理后大鼠肾组织纤维化、系膜基质增生、炎性浸润显著改善。结论PK可能通过改善大鼠肾脏血流动力学、抑制细胞凋亡来干预DN大鼠肾纤维化进程。Objective To explore effects of pancreatic kininogenase(PK)on renal fibrosis(RF)in rats with streptozotocin(STZ)-induced diabetic nephropathy(DN)and its mechanism.Methods Sixty male Wistar rats were collected and divided into healthy control group(Control),model group(Model),low-dose PK group(75 U/kg)and high-dose PK group(150 U/kg)by random number table method,15 cases in each group.Except healthy control group,STZ induction was performed to establish DN rats models.The tail-cuff method was applied to measure systolic blood pressure(SBP)of tail artery in each group.The changes in blood urea nitrogen(BUN),serum creatinine(SCr),nitric oxide(NO)andβ-2 microglobulin(β2-MG)were compared among all groups.The expression of renal apoptosis proteins Caspase-3 and Caspase-9 was detected by Western blotting.The pathological and morphological changes of renal tissues in each group were observed by PSAM-Masson staining.Results At weeks 3,6 and 9,SBP,BUN,SCr,β2-MG,Caspase-3 and Caspase-9 were significantly lower in 150 U/kg group than in Model group and 75 U/kg group(P<0.05);NO was significantly higher in 150 U/kg group than in Model group and 75 U/kg group(P<0.05).Masson staining results showed that compared with Model group,renal tissue fibrosis,mesangial matrix hyperplasia and inflammatory infiltration were significantly improved in each group treated with PK.Conclusion PK can treat RF in rats with STZ-induced DN.And its action mechanism may be related to improving renal hemodynamics and inhibiting renal cell apoptosis.

关 键 词：糖尿病肾病 胰激肽原酶 脑缺血 细胞凋亡 

分 类 号：R587.2[医药卫生—内分泌]