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5 mg/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24 h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24 h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。［中国当代儿科杂志，2010，12(11)：912-914］

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 (P<0.01). 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 (P<0.01). IL-6 expression in urine and renal tissues was positively correlated with 24-hour urinary protein excretion in the nephropathy group (r=0.794, P<0.01; r= 0.870, P<0.01). IL-6 expression in urine was positively correlated with that in renal tissues (r=0.739, P<0.01). 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.［Chin J Contemp Pediatr, 2010, 12 (11):912-914］