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目的探讨白藜芦醇预防小鼠高脂血症形成的作用效果及其分子机制。方法50只普通健康小鼠随机分成:①正常对照组;②高脂对照组;③白藜芦醇低剂量组〔50 mg/(kg.d)〕;④白藜芦醇中剂量组〔100 mg/(kg.d)〕;⑤白藜芦醇高剂量组〔150 mg/(kg.d)〕。白藜芦醇各实验组先普通饲养喂养2周,后转为高脂饲料喂养3周并同时按剂量给药;正常对照组一直普通饲料喂养5周;高脂对照组先普通饲料喂养2周,后转为高脂饲料再喂养3周。实验共观察5周,结束后处死小鼠并检测各组小鼠血清中TG、TC、LDL-C、HDL-C浓度及相关基因LDLR、angptl3 mRNA表达情况。结果①白藜芦醇各实验组可降低小鼠血清中TG、TC及LDL-C浓度,升高HDL-C浓度,与高脂对照组相比,差异有统计学意义(P<0.05);②白藜芦醇各实验组可促进LDLR基因mRNA表达增高,抑制angptl3基因mRNA表达,与高脂对照组相比,差异有统计学意义(P<0.05)。结论白藜芦醇能有效预防小鼠高脂血症的形成,其机制可能与下调angptl3、上调LDLR基因mRNA表达有关。
Objective To investigate the effect and mechanism of resveratrol on the prevention of hyperlipidemia in mice. Methods 50 normal healthy mice were randomly divided into: 1 normal control group; 2 high-fat control group; 3 low dose group of resveratrol [50 mg/(kg.d)]; 4 medium dose group of resveratrol [100 Mg/(kg.d)〕;5 Resveratrol high dose group [150 mg/(kg.d)]. Resveratrol in each experimental group was fed for 2 weeks, then fed with high-fat diet for 3 weeks and dosed at the same time. The normal control group was fed with common diet for 5 weeks, and the high-fat control group was fed with common diet for 2 weeks. After that, it was switched to high-fat diet and fed for another 3 weeks. The experiment was observed for a total of 5 weeks. After the end of the experiment, the mice were sacrificed and the serum TG, TC, LDL-C, HDL-C concentrations and related gene LDLR and angptl3 mRNA expression were detected in each group. Results 1 Resveratrol in each experimental group can reduce the concentration of TG, TC and LDL-C in the serum of mice, and increase the concentration of HDL-C. Compared with the high-fat control group, the difference was statistically significant (P<0.05); 2 Resveratrol in each experimental group promoted the mRNA expression of LDLR gene and inhibited the mRNA expression of angptl3 gene. Compared with the high-fat control group, the difference was statistically significant (P<0.05). Conclusion Resveratrol can effectively prevent the formation of hyperlipidemia in mice. The mechanism may be related to the down-regulation of angptl3 and up-regulation of LDLR gene mRNA expression.