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目的探讨盐酸二甲双胍联合辛伐他汀对奥氮平诱导性肥胖大鼠血糖、血脂代谢紊乱和肿瘤坏死因子-α的调节作用。方法 60只SD雄性健康大鼠随机分成模型组、盐酸二甲双胍联合辛伐他汀组(观察组)与对照组各20只,对照组给予普通饲料喂养,在普通饲料喂养基础上模型组给予奥氮平1.2mg/kg灌胃,观察组给予奥氮平1.2mg/kg、盐酸二甲双胍0.75g/d联合辛伐他汀10mg/d灌胃,4周后建立模型,检测3组空腹血糖、血脂生化和肿瘤坏死因子-α水平。结果模型组空腹血糖、总胆固醇、三酰甘油、低密度脂蛋白胆固醇及肿瘤坏死因子-α水平明显高于对照组和观察组(P<0.01),高密度脂蛋白胆固醇水平低于对照组与观察组(P<0.01);观察组空腹血糖、总胆固醇、三酰甘油、低密度脂蛋白胆固醇水平高于对照组,高密度脂蛋白胆固醇低于对照组(P<0.01),肿瘤坏死因子水平与对照组比较差异无统计学意义(P>0.05)。结论盐酸二甲双胍联合辛伐他汀具有降低奥氮平诱导性肥胖大鼠空腹血糖、肿瘤坏死因子-α水平及调节血脂的作用。
Objective To investigate the effects of metformin hydrochloride combined with simvastatin on the regulation of blood glucose and lipid metabolism and tumor necrosis factor-α in olanzapine-induced obese rats. Methods Sixty male SD rats were randomly divided into model group, metformin hydrochloride combined with simvastatin group (observation group) and control group (n = 20). The control group was fed with normal diet. On the basis of normal diet, the model group was given olanzapine 1.2mg / kg orally. The observation group was orally administered olanzapine 1.2mg / kg, metformin 0.75g / d combined with simvastatin 10mg / d orally, 4 weeks later, the model was established. The fasting blood glucose, serum lipid and tumor Necrosis factor-alpha levels. Results The levels of fasting blood glucose, total cholesterol, triglyceride, low density lipoprotein cholesterol and tumor necrosis factor-α in model group were significantly higher than those in control group and observation group (P <0.01), and the levels of high density lipoprotein cholesterol (P <0.01). The levels of fasting blood glucose, total cholesterol, triglyceride and low density lipoprotein cholesterol in the observation group were significantly higher than those in the control group, and the levels of high density lipoprotein cholesterol were lower than those in the control group (P0.01). The levels of tumor necrosis factor Compared with the control group, there was no significant difference (P> 0.05). Conclusions Metformin hydrochloride combined with simvastatin can reduce fasting blood glucose, tumor necrosis factor-α and regulate blood lipid in olanzapine-induced obese rats.