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目的:研究翻白草总黄酮对2型糖尿病大鼠糖脂代谢和肝组织胰岛素底物-2-磷脂酰肌醇-3激酶(IRS-2-PI3-K)信号通路的影响。方法:翻白草经溶剂提取,聚酰胺柱分离提取得总黄酮提取物;以高脂高糖乳剂加链脲佐菌素复制2型糖尿病大鼠模型,将造模成功的大鼠随机分为翻白草总黄酮高剂量(216 mg·kg﹣1)和低剂量(108 mg·kg﹣1)、模型对照组、阳性药组(盐酸二甲双胍悬浊液20.8 mg·kg-1),连续给药4周后,观察其血糖、血脂、游离脂肪酸、肝糖原、胰岛素水平的变化,采用Western blots法检测肝组织IRS-2和PI-3K蛋白的表达。结果:与正常组比较,模型组大鼠体重下降、血糖及总胆固醇(TC)升高;高密度脂蛋白胆固醇(HDL-C)下降(P<0.05)。与模型组比较,翻白草总黄酮高剂量组血糖下降(P<0.05),TC下降,HDL-C升高(P<0.05);胰岛素和胰岛素抵抗指数均降低(P<0.05);肝组织IRS-2和PI-3K蛋白的表达量升高(P<0.05)。结论:翻白草总黄酮能纠正2型糖尿病大鼠糖代谢紊乱,可能是通过降低减少肝糖原的输出,提高肝组织胰岛素IRS-2-PI3-K蛋白表达,从而减弱外周胰岛素抵抗。
OBJECTIVE: To study the effects of total flavonoids of Psidium Bluffn on glucose and lipid metabolism and IRS-2-PI3-K signal pathway in type 2 diabetic rats. METHODS: The extract of Pseudostellaria baicalensis was extracted by solvent and the total flavonoids was extracted by polyamide column. The model rats with type 2 diabetes were induced by high-fat and high-sucrose emulsion and streptozotocin, and the rats with successful model were randomly divided into The total flavonoids of Pseudostellariae Blossom were treated with high dose (216 mg · kg -1) and low dose (108 mg · kg -1) of the model group and the positive control group (20.8 mg · kg -1 of the metformin hydrochloride suspension) Four weeks later, the changes of blood glucose, blood lipid, free fatty acid, glycogen and insulin were observed. Western blotting was used to detect the expression of IRS-2 and PI-3K in liver tissues. Results: Compared with the normal group, the body weight, blood glucose and total cholesterol (TC) in the model group were significantly decreased and the level of HDL-C was decreased (P <0.05). Compared with the model group, the blood glucose of the high dosage group of Pseudostellariae Flavus decreased (P <0.05), TC decreased, the HDL-C increased (P <0.05), insulin and insulin resistance index decreased The expression of IRS-2 and PI-3K protein increased (P <0.05). Conclusion: The total flavonoids of Pseudostellaria baicalensis Georgi can correct the disorder of glucose metabolism in type 2 diabetic rats, which may be through reducing the output of hepatic glycogen and increasing the insulin IRS-2-PI3-K protein expression in liver tissue, thus attenuating the peripheral insulin resistance.