胰岛素增敏剂治疗高尿酸血症的初步研究

The sdudy of euglycemic agent to treatment hyperuricemia

目的:通过动物实验,验证胰岛素增敏剂治疗高尿酸血症的可行性,并从后者存在炎症反应和氧化应激的角度,探讨其作用的分子机制,为临床应用提供理论依据。方法:39只雄性WiStar大鼠随机分为正常对照组(简称正常组);高尿酸血症模型组;治疗组。采用高嘌呤饮食制造高尿酸血症模型,制模成功后分组,给予治疗组饲料中添加马来酸罗格列酮(文迪雅,格兰素史克公司出品)0.8mg/kg/d。各组治疗观察12周,同时正常组和模型组分别予相应饲料。检测大鼠血尿酸(UA)、血糖等,ELISA法检测血单核细胞趋化蛋白-1(MCP-1)、血8-异前列腺素F2α(8-iso-PGF2α)和肿瘤坏死因子-α(TNF-α)等。光镜观察大鼠肾脏的病理变化。结果:马来酸罗格列酮治疗后,与模型组比较,血糖、UA、MCP-1、8-iso-PGF2α、TNF-α明显下降(P值均<0.05、0.01)。大鼠肾脏病理显示改善。结论:胰岛素增敏剂马来酸罗格列酮可以降低高尿酸血症试验大鼠血糖、UA、MCP-1、8-iso-PGF2α、TNF-α等,其分子机制可能与抑制炎症和氧化应激有关。

Objective：To check the feasibility of euglycemic agentto treatment hyperuricemia by animal experiment. To investigate the molecule mechanism of treatment existing inflammatory reaction and oxidative stress, so to provide the basis of clinical application. Methods：68 WiStar male rats were divided into the normal control group,model group, treatment group. model group induced by high purine diet. normal control group and model group fed on common stoyer, treatment group added to rosiglitazone maleate （Avandia） 0.8mg/kg/d. After 12 weeks, blood uric acid, urine uric acid, serum glucose, microdosis urinary albumin were detected. MCP - 1,8 - iso - PGF2αand TNF - α were detected ELISA method. The pathological changes of the rats renal were observed with light microscope. Results： Compared with model group, after treatment with rosiglitazone maleate, serum glucose, uric acid, MCP - 1, 8 - iso - PGF2αand TNF -α were decreased significantly, pathological changes of the rats renal were improved. Conclusion： Euglyeemic agent rosiglitazone maleate could decrease serum glucose, uric acid, MCP - 1,8 - iso - PGF2α and TNF -α of hyperuricemia. The molecule mechanism perhaps is inhibiting inflamation and oxidative stress.