文献类型：期刊文献

英文题名：Long-term strength training causes a downregulation of nephrin in the slit diaphragm of kidneys in rats

作者：Niu, Yan-Long[1,2];Zhou, Hai-Tao[3];Guo, Xian[1];Wang, Yi[1];Cao, Jian-Min[1]

第一作者：Niu, Yan-Long

通讯作者：Cao, JM[1]

机构：[1]Beijing Sport Univ, Sport Sci Coll, 48 Xin Xi Rd, Beijing 100084, Peoples R China;[2]Gannan Med Univ, Sch Rehabil, Ganzhou 341000, Peoples R China;[3]Beijing Union Univ, Biochem Engn Coll, Beijing 100023, Peoples R China

第一机构：Beijing Sport Univ, Sport Sci Coll, 48 Xin Xi Rd, Beijing 100084, Peoples R China

通讯机构：[1]corresponding author), Beijing Sport Univ, Sport Sci Coll, 48 Xin Xi Rd, Beijing 100084, Peoples R China.

年份：2018

卷号：11

期号：7

起止页码：6965-6972

外文期刊名：INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000440379700061)】；

基金：This work was financially supported by 2016 Key laboratory projects of General administration of sport (Grant No. 2016SYS005); Collaborative innovation project of Beijing Chaoyang (Grant No. CYXC1508); Fundamental Research Funds for the Central Universities (Grant No. 2015YB009).

语种：英文

外文关键词：Strength training; slit diaphragm; nephrin; RAS

摘要：Objective: Excessive exercise causes an abnormality of the structure and function of the renal filtration barrier, which produces proteinuria. Our objective was to perform a study examining the molecular mechanism of sustaining exercise-induced proteinuria with cut point, combined with long-term strength training and nephrin in the slit diaphragm (SD) of the kidney. Methods: Male Sprague Dawley rats, aged 8 weeks, were divided into three groups. These groups included a control group (group A), an overload group drawn immediately (group C), and an overload group drawn after 24 hours (group D). A rat model of exercise-induced proteinuria was produced by long-term strength training, then we observed the glomerular structure, tested the nephrin protein expression of the kidney, and the intrarenal and circulating blood renin-angiotensin system (RAS). Results: The urine total protein (TP, P<0.01), microalbumin (mALB, P<0.01), and microalbumin/creatimne (mALB/CRE, P<0.01) of groups C and D are higher than that of group A. The abnormality of the glomerular structure of group C was obvious, and that of group D was slight The nephrin expression of group C (P<0.01) and group D (P<0.01) were lower than in group A. The intrarenal renin activity (Ra, P<0.01) and angiotension II (Angll, P<0.01) of group C were lower than that of group A, but the two groups had no differences in the circulating blood. The intrarenal Ra and Angll of group D were considerably higher than in group A and were the same in circulating blood. Conclusion: The intrarenal and circulating blood RAS were continuously active and induced by long-term strength training, which down regulated nephrin protein expression. This led to abnormalities of the structure and function of SD and resulted in proteinuria.