摘要
目的通过动物实验,验证胰岛素增敏剂治疗高尿酸血症及代谢综合征的可行性,并从二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68只雄性WiStar大鼠随机分为正常对照组(简称正常组)、模型组,、治疗组。采用高嘌呤和高嘌呤高脂高糖饮食制造高尿酸血症和代谢综合征模型,制模成功后分组,给于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)、尿尿酸、血糖、尿微量白蛋白等,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。结果马来酸罗格列酮治疗后,与模型组比较,治疗组血糖、UA、MCP-1、8-iso-PGF2α、TNF-α明显下降(P值均<0.05、0.01)。结论胰岛素增敏剂马来酸罗格列酮可以降低高尿酸血症及代谢综合征试验大鼠血糖、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 and metabolism syndrome 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, hyperuricemia and metabolism model induced by high purine and high purine,high lipoids and high glucose diet.normal control group and model group fed on common stoyer.treatment group added to rosiglitazone maleate (Avandia) 0.8 mg/kg/d. After 12 weeks, blood uric acid, urine uric acid, serum glucose, microdosis urinary albumin were detected. MCP-1, 8-iso-PGF2α and TNF-α were detected ELISA method. Result Compared with model group, after treatment with rosiglitazone maleate, serum glucose, uric acid, MCP-1, 8-iso-PGF2α and TNF-α were decreased significantly. Conclusion Euglycemic agent rosiglitazone maleate could decrease serum glucose, uric acid, MCP-1, 8-iso-PGF2α and TNF-α of hyperuricemia and metabolism syndrome.the molecule mechanism perhaps is inhibiting inflamation and oxidative stress.
出处
《临床医学工程》
2009年第5期8-10,共3页
Clinical Medicine & Engineering
关键词
胰岛素增敏剂
尿酸
代谢综合征
氧化应激
euglycemic agen
uric acid
metabolism syndrome
oxidative stress