首页> 中文期刊> 《中国中医药信息杂志》 >六黄合剂对胰岛素抵抗大鼠血管内皮细胞的影响

六黄合剂对胰岛素抵抗大鼠血管内皮细胞的影响

         

摘要

目的 观察六黄合剂对胰岛素抵抗(IR)大鼠血管内皮细胞的影响,探讨其保护血管内皮的作用机制.方法 健康SD大鼠32只,按体质量随机分为正常组、模型组、罗格列酮组和六黄合剂组,每组8只.应用地塞米松诱导IR大鼠模型,造模同时灌胃给药,罗格列酮组和六黄合剂组分别给予罗格列酮3 mg/(kg·d)和六黄合剂6.3 g/(kg·d)干预,正常组和模型组给予等体积蒸馏水,14 d后应用化学比色法测定大鼠脂代谢指标及血清一氧化氮(N0)的水平,应用透射电镜观察胸主动脉内皮细胞超微结构的变化.结果 与模型组比较,六黄合剂组血清三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)和游离脂肪酸(FFA)水平明显下降(P<0.01),血清总胆固醇(TC)水平下降(P<0.05),高密度脂蛋白胆固醇(HDL-C)水平升高(P>0.05),血清NO水平明显升高(P<0.01).电镜观察,IR大鼠胸主动脉内皮细胞超微结构发生明显病理改变.六黄合剂干预后,胸主动脉内皮细胞超微结构明显改善.结论 六黄合剂能有效调节IR大鼠血脂水平,增加血清NO含量,改善IR早期大动脉内皮细胞的病理损害.%Objective TO investigate the effects of Liuhuangheji on vascular endothelial cell in insulin resistant (IR) rats, and study its mechnism of vascular endothelium protection. Methods Thirty-two healthy SD rats were randomly divided into four groups: normal group, model group, rosiglitazon group and Liuhuangheji group, according to body weight, 8 rats in each group. The model of IR rats was induced with dexamethasone. Rosiglitazon group and Liuhuangheji group were given rosiglitazon 3 mg/(kg · d) and Liuhuangheji 6.3 g/(kg · d) respectively, and other groups were given the same volume distilled water. Serum lipid and NO were determined by the chemical colorimetry after 14 days. Ultrastructure of aortic endothelial cells was observed with transmission electron microscope. Results TG, LDL-C and free fatty acid (FFA) in Liuhuangheji group were significantly lower than those in model group (both P<0.01), and serum TC decreased (P<0.05). Serum level of HDL-C in Liuhuangheji group was higher than those in model group, but without significant difference (P>0.05). NO level significantly increased in Liuhuangheji group (P<0.01). The aortic endothelial cells in model group showed pathologic changes of ultrastructure by electron microscope. The ultrastructure of aortic endothelial cells in Liuhuangheji group improved obviously. Conclusion Liuhuangheji can effectively regulate serum lipid level, increase serum NO level, and protect aortic endothelial cell from dexamethasone-induced damage in IR rats at early stage of IR.

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