标题：Simvastatin ameliorates renal lipidosis through the suppression of renal CXCL16 expression in mice with adriamycin-induced nephropathy
作者：Wang, Cong; Li, Qian; Zhen, Junhui; Xu, Yihuai; Sun, Shuzhen
作者机构：[Wang, Cong; Li, Qian; Xu, Yihuai; Sun, Shuzhen] Shandong Univ, Shandong Prov Hosp, Dept Pediat Nephrol & Rheumatism & Immunol, Jinan, Shandong, Peopl 更多
通讯作者地址：[Sun, SZ]Shandong Univ, Dept Pediat Nephrol & Rheumatism & Immunol, Shandong Prov Hosp, 324 Jing Wu Rd, Jinan, Shandong, Peoples R China.
来源：INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
关键词：Balb/c mice; adriamycin; nephropathy; CXCL16; ox-LDL; simvastatin
摘要：Aims: To investigate the roles of CXCL16 and ox-LDL in adriamycin (ADR)-induced nephropathy mice and to explore the mechanism of simvastatin on the renal protective effects of ADR nephropathy. Methods: Fifteen male Balb/c mice were randomly divided into normal control (NC), ADR nephropathy and simvastatin-treated ADR nephropathy (ADR-SIM) groups. ADR nephropathy was induced by a single intravenous injection of ADR into the tail vein. All mice were sacrificed at the end of the 7th week, with the blood, 24-h urine and kidneys collected. The levels of ox-LDL and total cholesterol in the serum, the serum CXCL16, ox-LDL and NF-kappa B expression were detected. Results: Compared with the NC group, the levels of serum total cholesterol and ox-LDL in the ADR and ADR-SIM groups were significantly higher, the level of serum albumin was significantly lower and the expression of CXCL16, ox-LDL and NF-kappa B in the renal tissue of ADR and ADR-SIM groups was significantly increased. Compared with the ADR group, the expressions of renal CXCL16, ox-LDL and NF-kappa B in the ADR-SIM group were significantly decreased. Levels of serum total cholesterol and ox-LDL were not significantly different between the two groups. Conclusions: Simvastatin exerts a protective effect on renal function and structure in mice with ADR nephropathy. The beneficial effects of simvastatin might be related to the decreasing expression of CXCL16 in glomerular podocytes followed by the decreasing endocytosis of ox-LDL in podocytes and inhibition of NF-kappa B pathway activation.