摘要
目的:观察复方土茯苓颗粒对高尿酸血症肾病模型小鼠血尿酸、肾功能的影响及肾脏组织中白细胞介素1(IL-1β)、白细胞介素6(IL-6)表达的影响。方法:采用腺嘌呤(100 mg.kg-1)联合97%氧嗪酸钾(1 g.kg-1)ig法建立小鼠高尿酸血症肾病动物模型,设立正常对照组、造模组、阳性药物组苯溴马隆组20 mg.kg-1、复方土茯苓颗粒高、中、低剂量组(6,3,1.5 g.kg-1)。实验第21天小鼠眼球采血后处死,检测血清中尿酸、肌酐、尿素氮及肾组织中IL-1β,IL-6水平。结果:复方土茯苓颗粒高、中、低剂量组尿酸(110.22±28.07),(128.10±54.79)(144.10±51.73)μmol.L-1;肌酐(39.11±8.55),(60.90±21.29),(87.50±16.18)μmol.L-1;尿素氮(25.15±3.17),(29.65±2.17),(35.01±3.63)mmol.L-1;IL-1β(3.13±0.53),(4.26±1.44),(5.10±1.86)μg.L-1;IL-6(14.90±4.93),(22.87±6.71),(35.83±22.19)μg.L-1;与模型组血尿酸(259.22±31.05)μmol.L-1、肌酐(103.00±22.34)μmol.L-1,尿素氮(50.76±9.93)mmol.L-1,IL-1β(10.74±4.0)μg.L-1,IL-6(62.87±15.42)μg.L-1相比明显降低(P<0.05),复方土茯苓颗粒高、中剂量组与苯溴马隆组相比,组间比较无统计学差异。结论:复方土茯苓颗粒能够有效降低高尿酸血症肾病模型小鼠尿酸、肌酐、尿素氮水平,保护尿酸造成的肾脏损伤,可能机制为降低IL-1β,IL-6等炎症因子的表达。
Objective: To observe the effect of Fufang Tufuling granules on serum level of uric acid (UA), Urea nitrogen (BUN), creatinine (Cr), and the level of interleukin 1β(IL-1β), interleukin 6 (IL-6) in mouse kidriey homogenate. Method: Animal model was made by Adenine (100 mg·kg^-1) and uricase (1 g·kg^-1). The animals were divided into normal group, model group, positive drug Benzbromarone 20 mg·kg^-1 group, Fufang Tufuling granules high dose group, Fufang Tufuling granules middle dose group, Fufang Tufuling granules low dose group (6, 3, 1.5 g·kg^-1 ). At the 21th day, blood was collected, then the serum level of UA, BUN, CR, and the IL-1β, IL-6 in Kidney homogenate were measured. Result: The serum level of UA [ (110.22±28.07), (128.10±54.79), (144.10±51.73) μg·L^-1], BUN [ (25.15±3.17, (29.65± 2.17), (35.01±3.63) mmol·L^-1], Cr [ (39.11 ±8.55) , (60.90±21.29) , (87.50 ±16. 18)μg·L^-1], and the level oflL-1β [ (3.13±0.53) , (4.26±1.44) , (5.10±1.86)μg·L^-1], IL-6 [ (14.90±4.93), (22.87±6.71 ), (35.83±22. 19) μg·L^-1 in kidney homogenate in Fufang Tufuling granules high, middle and low dose group was lower than those in the model group (P 〈 0.05). The effects of high and medium dose group were similar to Benzbromarone group. Conclusion: The Fufang Tufuling granules can prevent and cure experimental hyperuricemia and hyperuricemic renal impairment. The mechanism might be related to inhibiting the expressions of IL-1β and IL-6.
出处
《中国实验方剂学杂志》
CAS
北大核心
2012年第16期191-194,共4页
Chinese Journal of Experimental Traditional Medical Formulae
基金
全军"十一五"计划专项基金项目(2006062004)
广东省科技计划项目(2009B030801277)
广州市科技计划项目(2010GN-E00221)