标题 | 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 |
范文 | 李丹丹 刘佳佳 吴玉泓 李海龙 王勇 陈彻 王晶 摘要: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,衰老对照組糖原、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。 关键词:衰老2型糖尿病;二甲双胍;黄芪多糖;肝脏;糖脂代谢;小鼠 中图分类号:R285.5 ???文献标识码:A??? 文章编号:1005-5304(2019)02-0047-05 DOI:10.3969/j.issn.1005-5304.2019.02.011 开放科学(资源服务)标识码(OSID): Abstract: 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. Keywords: aging type 2 diabetes; metformin; astragalus polysaccharides; liver; glucose and lipid metabolism; mice [1] YEHUDA A B, ZINGER A. The older patient with diabetes: a practical approach[J]. Diabetes/metabolism Research & Reviews, 2014,30(2):88-95. [2] 李永民,李建东,杨洁,等.中药糖平煎对实验性2型糖尿病治疗机理的研究[C]//中华中医药学会内科分会消渴病学术研讨会,2003. [3] 毛竹君,寿旦,柴可夫.黄芪多糖小檗碱下调IR-INS-1细胞miR-126-3p改善胰岛素抵抗[J].中华中医药杂志,2017,32(7):2961-2965. [4] 唐思梦,杨泽民,陈伟强,等.黄芪多糖保护胰岛β细胞改善大鼠2型糖尿病[J].第二军医大学学报,2017,38(4):482-487. [5] 胡彩虹,徐坤,孙静,等.黄芪多糖对老年糖尿病大鼠糖脂代谢的影响[J].中国老年学杂志,2018,38(6):1453-1455. [6] 许芳芳,王楠,李刚强,等.2型糖尿病小鼠模型的建立与评价[J].中国医学科学院学报,2017,39(3):324-329. [7] 王晶,黄勇,李海龙,等.党参水提物对D-半乳糖致衰老小鼠肾组织microRNA表达谱的影响[J].中国中医药信息杂志,2016,23(5):69-72. [8] 章常华,刘彤彤,邓可众,等.黄芩-黄连药对防治D-半乳糖痴呆小鼠的作用机制[J].中成药,2018,40(3):524-529. [9] 刘克明,王春花,李国星,等.D-半乳糖模型鼠与自然衰老鼠的比较研究[J].卫生研究,2007(6):685-688. [10] 黄桂红,陈薇,罗昱澜.链脲佐菌素稳定性对诱导糖尿病小鼠模型的影响[J].华夏医学,2009,22(2):201-203. [11] NOVELLE M G, ALI A, DIEGUEZ C, et al. Metformin:A hopeful promise in aging research[J]. Cold Spring Harbor Perspectives in Medicine,2016,6(3):a025932. [12] 常越,徐姣,闫嵩,等.黄芪六一汤对2型糖尿病治疗效果的转录组学研究[J].中国中药杂志,2017,42(14):2760-2766. |
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