白细胞介素-6在多柔比星肾病大鼠模型中的表达及意义

Expression of interleukin-6 in rat model of doxorubicin-induced nephropathy

目的微小病变型肾病(MCNS)的发病机制目前尚不明确,故对其机制的研究显得尤为重要,该研究旨在探讨白细胞介素-6(IL-6)在多柔比星肾病大鼠模型中的表达和意义。方法雄性Wistar大鼠83只随机分为正常组(32只)、肾病组(51只)。肾病组一次性尾静脉注射多柔比星5mg/kg,建立多柔比星肾病模型,正常组注射等量生理盐水,于注射多柔比星后第7、14、28、42天检测各组大鼠24h尿蛋白定量,并分批处死大鼠,采用酶联免疫吸附(ELISA)法检测各组大鼠不同时期尿液及肾组织中IL-6的表达。结果肾病组大鼠尿蛋白排泄量随着注射后时间的延长逐渐增加,第7、14、28、42天与正常组比较,差异均有统计学意义(P<0.01)。第7、14、28、42天肾病组大鼠肾组织及尿液中IL-6表达明显增加,与正常组比较,差异均有统计学意义(P<0.01)。肾病组尿及肾组织中IL-6的表达与24h尿蛋白的排泄量呈正相关(r=0.794,P<0.01;r=0.870,P<0.01)。肾组织及尿液中IL-6的表达呈正相关(r=0.739,P<0.01)。结论 IL-6在MCNS大鼠尿液及肾脏组织中存在异常表达。IL-6可能在MCNS的发生发展中起重要作用。

Objective The pathogenesis of minimal change nephrotic syndrome（MCNS） remains unclear.This study aimed to investigate the expression of interleukin-6（IL-6） in rats with doxorubicin-induced nephropathy and its possible roles in the pathogenesis of MCNS .Methods Eighty-three male Wistar rats were randomly assigned into a control group（n=32） and a nephropathy group（n=51） .Nephropathy was induced by a single tail vein injection of doxorubicin（5 mg/kg）.The control group was injected with normal saline.Twenty-four-hour urinary protein excretion was measured 7,14,28 and 42 days after doxorubicin injection.IL-6 expression in urine and renal tissues was determined using ELISA 7,14,28 and 42 days after doxorubicin injection.Results The urinary protein excretion increased significantly in the nephropathy group 7,14,28 and 42 days after doxorubicin injection compared with that in the control group（P0.01）.IL-6 expression in urine and renal tissues increased significantly 7,14,28 and 42 days after doxorubicin injection compared with that in the control group（P0.01）.IL-6 expression in urine and renal tissues was positively correlated with 24-hour urinary protein excretion in the nephropathy group（r=0.794,P0.01;r= 0.870,P0.01）.IL-6 expression in urine was positively correlated with that in renal tissues（r=0.739,P0.01）.Conclusions IL-6 expression in the urine and renal tissues is increased in MCNS rats.IL-6 might play an important role in the pathogenesis of MCNS.