金芪降糖片对胰岛素抵抗大鼠肝脏SREBP-1c mRNA表达的影响

The Effect of Jinqi Jiangtang Pian on SREBP-1c mRNA Expression in Liver of Insulin-Resistant Rats

目的:探讨金芪降糖片干预胰岛素抵抗(IR)的疗效及分子机制。方法:将Wistar大鼠27只随机分为普通喂养(NC)组(9只)和模型(MG)组(18只),普通喂养组予普通饲料喂养,模型组予高脂饲料喂养建立IR模型。8周后将成模大鼠随机分成高脂饮食(HF)组和高脂饮食+金芪降糖(HF+JQ)组,各9只。HF+JQ组予金芪降糖(2.1g·kg-·1d-1)灌胃,NC组和HF组均予生理盐水灌胃,6周后取静脉血测定血糖、胰岛素、三酰甘油(TG)、游离脂肪酸(FFA)、血清肿瘤坏死因子-α(TNF-α)、瘦素等指标,计算胰岛素敏感指数(ISI)。取肝脏组织采用RT-PCR法检测SREBP-1c mRNA表达。结果:与NC组相比,HF组大鼠ISI降低,肝脏SREBP-1c mRNA表达增加(均P<0.01)。与HF组相比,HF+JQ组大鼠TG、FFA及血清瘦素、TNF-α均明显降低,ISI升高,肝脏SREBP-1c mRNA表达降低(均P<0.01)。结论:金芪降糖能抑制IR大鼠肝脏SREBP-1c的过度表达,有效改善IR。

Objective：To investigate the therapeutic effect and mechanism of Jinqi Jiangtang Pian on insulin resistance （IR）. Methods：Twenty-seven Wistar rats were randomly divided into two groups. Rats were fed with high-fat diet for 8 weeks to establish IR rat model（n = 18）. Rats were fed with common diet in normal control group（n = 9）. The rats in model group were randomly subdivided into two groups,high-fat-feeding group （HF, n = 9） and high-fat-feeding＋Jinqi Jiangtang Pian group （HF＋JQ, n = 9）. The rats of HF＋JQ group were lavaged with Jinqi Jiangtang Pian （2.1 g·kg-1·d-1）. Rats were lavaged with normal saline in HF group and normal control group. The serum concentrations of insulin, glucose, triglyceride（TG）, free fatty acid （FFA）, TNF-α and leptin were measured in all rats after another 6 weeks feeding. The insulin sensitive index （ISI） was calculated. The expression of SREBP-1c mRNA in the liver tissue was detected with real time polymerase chain reaction（RT-PCR）. Results： Compared with normal control group, ISI was decreased obviously in HF group （P 0.01）,and SREBP-lc mRNA expression was upregulated in the liver tissue（P 0.01）. Compared to HF group, the serum levels of TG, FFA, leptin and TNFα were significantly decreased in HF＋JQ group （P 0.01） while ISI was increased （P 0.01）. In addition, SREBP-1c mRNA expression was downregulated in the liver tissue of HF＋JQ group （P 0.01）. Conclusion： Jinqi Jiangtang Pian can inhibit the expression of SREBP-1c mRNA, and improve IR in the liver of high-fat-fed rats.