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目的观察CXC趋化因子配体16(CXCL16)和氧化低密度脂蛋白(ox-LDL)在阿霉素肾病小鼠中表达的变化及其与肾组织形态学的关系,探讨辛伐他汀对阿霉素肾病肾脏保护作用的机制。方法将15只雄性Balb/c小鼠分为正常对照组、阿霉素肾病组、辛伐他汀治疗组,每组5只,分别进行相应处理。5周后留取血液、24 h尿液,进行一般生化指标及血清ox-LDL的检测;此后处死小鼠,摘取肾脏组织,采用光镜、电镜和双重免疫荧光技术分别观察肾组织形态结构、超微结构和CXCL16、ox-LDL的表达。结果与正常对照组相比,阿霉素肾病组与辛伐他汀治疗组小鼠血清总胆固醇和ox-LDL水平升高,肾组织CXCL16、ox-LDL表达增强(P均<0.05)。与阿霉素肾病组相比,辛伐他汀治疗组小鼠肾组织CXCL16、ox-LDL表达均有不同程度的降低(P均<0.05),但血清总胆固醇和ox-LDL水平没有明显下降。相关分析显示,肾组织CXCL16表达水平与肾组织病理学慢性指数、肾组织ox-LDL水平呈明显正相关(r=0.92,P<0.01;r=0.97,P<0.01)。结论辛伐他汀可能通过抑制肾小球足细胞CXCL16的表达,进而减少足细胞对ox-LDL的摄取而发挥肾脏保护作用。
Objective To investigate the expression changes of CXCL16 and ox-LDL in doxorubicin-induced nephropathy mice and its relationship with renal histomorphology. To investigate the effects of simvastatin on Mechanism of kidney protection in nephrotic syndrome. Methods Fifteen male Balb / c mice were divided into normal control group, adriamycin nephropathy group and simvastatin treatment group, with 5 rats in each group. After 5 weeks, blood and 24 h urine were collected for detection of general biochemical parameters and serum ox-LDL. Afterwards, mice were killed and their kidneys were harvested. Morphology and structure of kidney were observed by light microscope, electron microscope and double immunofluorescence , Ultrastructure and CXCL16, ox-LDL expression. Results Compared with the normal control group, the levels of serum total cholesterol and ox-LDL in adriamycin nephropathy group and simvastatin treatment group were increased, and the expressions of CXCL16 and ox-LDL in renal tissue were increased (all P <0.05). Compared with adriamycin-induced nephropathy group, the expression of CXCL16 and ox-LDL in simvastatin group decreased to some extent (all P <0.05), but serum total cholesterol and ox-LDL levels did not decrease significantly. Correlation analysis showed that the expression of CXCL16 in renal tissue was positively correlated with the chronic pathological indexes of kidney and ox-LDL in renal tissue (r = 0.92, P <0.01; r = 0.97, P <0.01). Conclusion Simvastatin may exert renal protective effect by inhibiting the expression of glioma podocyte CXCL16, thereby reducing the uptake of ox-LDL by podocytes.