人参皂苷Rg1对多柔比星肾病大鼠足细胞nephrin的影响

目的足细胞的损伤是蛋白尿发生的主要机制,如何修复受损的足细胞已成为研究热点。文中观察人参皂苷Rg1对足细胞病变模型———多柔比星肾病模型的疗效及其对足细胞病变的影响。方法采用单次尾静脉注射盐酸多柔比星建立多柔比星肾病模型。SD大鼠分为空白对照组、模型组、人参皂苷Rg1高剂量组和低剂量组,分别在注射后第7、14、28天收集尿液标本,并处死大鼠,留取肾组织标本。检测24 h尿蛋白排泄量、血生化指标,行肾组织光镜和电镜观察肾小球病变和足突超微结果。采用定量学方法测定足突宽度。免疫组化观察足细胞裂孔膜分子nephrin表达和分布变化。结果人参皂苷Rg1低剂量组和高剂量组均能改善多柔比星肾病大鼠的肾病综合征状况。同时,人参皂苷Rg1低剂量组和高剂量组能明显改善足突融合,增加足细胞裂孔膜分子nephrin表达(P<0.05)。人参皂苷Rg1高剂量组在血生化、肾脏病理和足细胞nephrin的表达上比人参皂苷Rg1低剂量组的改善更加明显(P<0.05)。结论人参皂苷Rg1对多柔比星肾病模型有很好的保护作用,而且人参皂苷Rg1高剂量组比低剂量组治疗作用更明显。

Ginsenoside Rg1 increases the expression of nephrin in adriamycin-induced nephrotic rats

Objective Podocyte injury is believed to be a major contributor to proteinuria,and therefore how to repair damaged podocytes has become a focus of research in recent years.The aim of this study was to investigate the therapeutic effects of ginsenoside Rg1 on adriamycin(ADR)-induced nephrotic syndrome in rats and its protection against on podocyte injuries.Methods Thirty-two SD rats were divided randomly into a blank control,an ADR nephrosis model,a low-dose ginsenoside Rg1 and a high-dose ginsenoside Rg1 group.The model of ADR-induced nephrosis was established by single intravenous injection of ADR.Urine samples were collected and renal tissues were processed at 7,14 and 28 days.The 24h urinary protein excretion and blood biochemistry parameters were measured by routine methods.The glomerular morphology and podocyte ultrastructure were observed by light microscopy and transmission electron microscopy,respectively.The foot process width was determined by quantitative method,and the changes in the nephrin expression and distribution observed by immunohistochemistry.Results Both low-and high-dose ginsenoside Rg1 significantly improved the ADR-induced nephritic syndrome of the rats,and remarkably reduced the degree and area of podocyte foot process effacement.It also markedly increased the expression and distribution of nephrin,more significantly in the high-dose than in the low-dose group.Conclusion Ginsenoside Rg1 could protect the kidney against ADR-induced injury,more significantly at a high dose than at a low dose.