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目的:探讨亚硒酸钠对糖尿病肾病大鼠肾脏脂联素表达的影响及二者间的关系,从而研究亚硒酸钠和脂联素在糖尿病肾病中的作用机制。方法:通过链脲佐菌素法并给予高脂饮食诱导模拟大鼠糖尿病肾病模型,实验设空白对照组、糖尿病肾病对照组、亚硒酸钠干预组,每组10只。亚硒酸钠干预组每日给予亚硒酸钠溶液1μg/kg灌胃,其他各组给予等量盐水溶液灌胃。灌胃10周后处死大鼠,取大鼠血、尿标本测相关生化指标。快速切取小块肾皮质组织,4%戊二醛固定,制电镜切片扫描电镜观察超微结构。取肾脏组织标本制石蜡切片光镜下观察病理改变及免疫组化分析定位蛋白表达,定量PCR法检测脂联素的mRNA表达、蛋白质印迹法检测脂联素蛋白表达。结果:亚硒酸钠干预组大鼠基本状况和生化指标较糖尿病肾病对照组明显改善,光镜下亚硒酸钠干预组病理改变和电镜下超微结构较糖尿病肾病对照组明显减轻。免疫组化分析,亚硒酸钠干预组脂联素蛋白着色较糖尿病肾病对照组明显增强,且肾小管、肾小球内均有着色。亚硒酸钠干预组脂联素mRNA是空白对照组的2.043倍,糖尿病肾病对照组脂联素mRNA是空白对照组的1.373倍。亚硒酸钠干预组脂联素蛋白表达水平高于糖尿病肾病对照组及空白对照组,差异有统计学意义(P<0.05)。结论:亚硒酸钠通过抗氧化应激、增加外周组织对胰岛素的敏感性从而促进肾脏脂联素表达,表明亚硒酸钠和脂联素在延缓和防治糖尿病肾病的发生发展中可能起重要作用。
AIM: To investigate the effect of sodium selenite on the expression of adiponectin in diabetic nephropathy rats and the relationship between them, so as to study the mechanism of action of sodium selenite and adiponectin in diabetic nephropathy. Methods: The model of diabetic nephropathy was induced by streptozotocin (STZ) and given a high fat diet. The blank control group, diabetic nephropathy control group and sodium selenite intervention group were randomly divided into 10 groups. Sodium selenite intervention group given daily sodium selenite solution 1 g / kg gavage, the other groups were given equal volume of saline solution gavage. After 10 weeks of gavage, rats were sacrificed and blood and urine samples were taken for determination of relevant biochemical parameters. Quickly cut a small piece of renal cortex tissue, 4% glutaraldehyde fixation, electron microscopy section scanning electron microscopy ultrastructure. The pathological changes were observed under light microscope and immunohistochemistry. The mRNA expression of adiponectin was detected by quantitative PCR. The expression of adiponectin protein was detected by Western blotting. Results: The basic status and biochemical indexes of rats in the sodium selenite intervention group were significantly improved compared with the diabetic nephropathy control group. The pathological changes of the rats treated with sodium selenite under light microscope and the ultrastructure of the rats treated with sodium selenite were significantly less than those of the diabetic nephropathy control group. Immunohistochemical analysis, sodium selenite intervention group adiponectin protein staining compared with diabetic nephropathy control group was significantly enhanced, and tubular, glomerular staining. Adiponectin mRNA was 2.043 times of that of the blank control group and 1.373 times of the adiponectin mRNA of diabetic nephropathy control group. The expression of adiponectin in sodium selenite intervention group was higher than that in diabetic nephropathy control group and blank control group, the difference was statistically significant (P <0.05). Conclusion: Sodium selenite can promote the expression of adiponectin in kidney through anti-oxidative stress and increase the sensitivity of peripheral tissues to insulin, indicating that sodium selenite and adiponectin may play an important role in the delay and prevention and treatment of diabetic nephropathy effect.