中文摘要：

目的研究鲫鱼汤对阿霉素肾病大鼠IL-17、IL-23、IL-1β和CXCR2等表达的影响，探讨其治疗作用和机制。方法成年Wistar雄性大鼠40只，随机分为鲫鱼汤组、厄贝沙坦组、肾病组、空白对照组，除空白对照组，其他三组给予尾静脉注射6．2mg／kg体重阿霉素建立肾病模型，空白组注射等容量生理盐水。模型成功后，给予鲫鱼汤灌胃干预9周，每周检测12h尿蛋白定量，检测终末血生化指标变化，光镜下观察大鼠肾脏病理改变，免疫组化检测IL-17、IL-23、IL-1β和CXCR2在肾脏的表达，ELISA法检测IL-17、IL-23和IL-1β在血液中的含量。结果鲫鱼汤组大鼠血白蛋白水平高于肾病组（P=0．03）低于空白组（P=0．01）；鲫鱼汤组大鼠肾组织IL-17、IL-23、CX-CR2较肾病组表达减少（P=0．01，P=0．01，P=0．02），较空白组表达增多（P=0．04，P=0．007，P=0．05）。结论Thl7细胞相关炎性因子增多是阿霉素肾病大鼠的发病机制之一，鲫鱼汤可通过升高血白蛋白，降低IL-17、IL-23、CXCR2表达而发挥肾脏保护作用。

英文摘要：

Objective To observe the therapeutic effect of Crucian carp decoction on rats with nephrosis in- duced by adriamycin, and explore its mechanism of action. Methods Fourty healthy 8-week old male Wistar rats were randomly divided into crucian carp decoction group, Irbesartan group, nephrosis group, and control group. The rat model of nephrosis was induced by a single tail vein injection of adriamycin 6.2 mg/kg body weight. The rats of the crucian carp decoction group were given oral gavage of crucian carp decoction once everyday for 9 weeks, and urinary protein was checked each week. All rats were killed at week 9. Histological changes were observed by light microscopy and blood bio- chemical indices were detected. IL-17, IL-23, IL-113, and CXCR2 expressions in the kidney were assessed by immunohis- tochemistry, Serum IL-17, IL-23, IL-113 levels were assayed by ELISA. Result Rats in the crucian carp decoction group had a higher level of albumin compared with that of the nephrosis group （ P = 0.03 ） , significantly lower than that of the control group（P = 0.01 ） and the expressions of IL-17, IL-23, and CXCR2 in the kidney were significantly lower than those in the nephrosis group （P = 0. 01,P = 0.01 ,P = 0. 02）, significantly higher than those of the control group （P = 0.04,P = 0. 007,P = 0.05）. Conclusions The increase of Th17 ceil inflammatory factors may be one of the pathogenetie mechanisms in rats with adriamycin-induced nephrosis. Crucian carp decoction can improve the albumin level of rats with nephrosis, and alleviate renal impairment induced by IL-17, IL-23 and CXCR2.