黄芪多糖联合二甲双胍对衰老2型糖尿病模型小鼠肝脏糖脂代谢的影响

Effects of Astragalus Polysaccharides Combined with Metformin on Glucose and Lipid Metabolism in Liver of Aging Type 2 Diabetic Mice

目的观察黄芪多糖联合二甲双胍对衰老2型糖尿病模型小鼠肝脏糖脂代谢的影响,探讨其作用机制。方法采用高糖高脂饲料联合链脲佐菌素诱导自然衰老小鼠制作衰老2型糖尿病小鼠模型。实验小鼠分为衰老对照组、衰老糖尿病模型组、二甲双胍治疗组、黄芪多糖+二甲双胍治疗组,各给药组给予相应药物灌胃,连续60 d。测定小鼠体质量、摄食、饮水、空腹血糖变化,HE染色观察小鼠肝组织形态学,糖原染色和油红O染色观察肝组织糖脂代谢,透射电子显微镜观察小鼠肝组织细胞超微形态。结果与衰老对照组比较,衰老糖尿病模型组空腹血糖明显升高、体质量减轻、摄食和饮水明显增加(P<0.05)。与衰老糖尿病模型组比较,各给药组空腹血糖明显降低、体质量增加、摄食和饮水明显减少(P<0.05)。HE染色显示,与衰老对照组比较,衰老糖尿病模型组肝组织病变、坏死严重,各给药组较模型组明显改善,其中黄芪多糖+二甲双胍治疗组肝组织结构改善最明显。糖原染色与油红O染色显示,衰老对照组糖原、脂滴含量较少,衰老糖尿病模型组糖原、脂滴含量明显增多;与衰老糖尿病模型组比较,各给药组小鼠肝组织糖原和脂滴含量均显著减少(P<0.05),且黄芪多糖+二甲双胍治疗组效果更明显。透射电镜观察显示,衰老糖尿病模型组较衰老对照组肝组织细胞线粒体、内质网损伤严重,各治疗组较模型组明显缓解,且黄芪多糖+二甲双胍治疗组效果更明显。结论黄芪多糖+二甲双胍可通过对肝组织细胞线粒体及内质网的保护作用,改善衰老2型糖尿病小鼠模型的肝脏糖脂代谢。

Objective To observe the effects of astragalus polysaccharides combined with metformin on liver glucose and lipid metabolism in aging type 2 diabetic mice;To discuss the mechanism of action. Methods The models of aging type 2 diabetic mice were induced by high sugar and high fat diet combined with streptozotocin in natural aging mice. The experimental mice were divided into aging control group, aging diabetic model group, metformin treatment group and astragalus polysaccharides combined with metformin treatment group. Each administration group was given the corresponding medicine for gavage for 60 days. The changes of body weight, feeding, drinking water and fasting blood glucose were measured in each group. The morphological changes of liver tissues were observed by HE staining. Glycogen staining and oil red O staining were performed to observe the glycolipid metabolism of liver tissue. Transmission electron microscopy was used to observe the ultrastructural changes of liver cells. Results Compared with the aging control group, the fasting blood glucose increased significantly, the body weight decreased and the feeding and drinking water increased significantly in the aging diabetic model group(P<0.05). Compared with the aging diabetic model group, the fasting blood glucose decreased significantly, the body weight increased, and the feeding and drinking water decreased significantly in each administration group(P<0.05). HE staining showed that compared with the aging control group, pathological changes and necrosis of the liver tissue in the aging diabetic model group were more serious, but the administration groups were significantly improved compared with the model group. The improvement of liver tissue structures in astragalus polysaccharides combined with metformin treatment group was the most obvious. Glycogen staining and oil red O staining showed that the contents of glycogen and lipid droplets in the aging control group were fewer, and the contents of glycogen and lipid droplets in the aging diabetic model group increased significantly(P<0.05). Compared with the aging diabetic model group, the contents of glycogen and lipid droplets in the liver tissues of the administration groups were significantly reduced(P<0.05), and in the astragalus polysaccharide combined with metformin treatment group, the reductions were more obvious. Transmission electron microscopy showed that the mitochondria and endoplasmic reticulum in the liver tissue of the aging diabetic model group had more damage rather than those in the aging control group, and the administration groups were significantly relieved compared with the aging model group, and the effects of astragalus polysaccharide combined with metformin were better. Conclusion Astragalus polysaccharide combined with metformin can improve glucose and lipid metabolism of liver in aging type 2 diabetic mice models by protecting liver mitochondria and endoplasmic reticulum.