黄芪多糖联合格列美脲对链脲佐菌素诱导的糖尿病小鼠认知功能障碍的保护作用  

Protective Effect of Astragalus Polysaccharide Combined with Glimepiride on Cognitive Dysfunction in Diabetic Mice Induced by Streptozotocin

作　　者：吴坚[1] 付瑛[2] WU Jian;FU Ying(Ganzhou People's Hospital,Ganzhou Jiangxi 341000,China;Qingdao Municipal Hospital,Qingdao Shandong 266500,China)

机构地区：[1]赣州市人民医院,江西赣州341000 [2]青岛市市立医院,山东青岛266500

出　　处：《药品评价》2021年第15期909-913,共5页Drug Evaluation

基　　金：赣州市指导性科技计划任务(GZ2018ZSF293)。

摘　　要：目的:分析黄芪多糖联合格列美脲对链脲佐菌素(STZ)诱导的糖尿病小鼠认知功能障碍的保护作用。方法:选取雄性ICR小鼠40只,分为正常对照组、模型组、格列美脲组、黄芪多糖联合格列美脲组(联合组),除正常对照组外其余小鼠均给予腹腔注射STZ建立糖尿病小鼠模型,各给药组给予相应药物灌胃,连续6周。测定小鼠体质量、空腹血糖变化;Morris水迷宫实验观察小鼠空间学习记忆能力;透射电镜观察各组小鼠胰岛β细胞、海马组织神经元超微结构;检测小鼠海马组织葡萄糖依赖性促胰岛素多肽(GIP)和胰高血糖素样肽-1(GLP-1)含量;检测小鼠脑组织超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量。结果:给药处理后,格列美脲组、联合组小鼠体质量较模型组明显升高,空腹血糖较模型组明显降低(P<0.05),且联合组小鼠体质量明显高于格列美脲组、空腹血糖明显低于格列美脲组(P<0.05)。自第4天开始格列美脲组、联合组小鼠逃避潜伏期明显短于模型组(P<0.05);格列美脲组、联合组小鼠穿越平台次数明显高于模型组(P<0.05),且联合组明显高于格列美脲组(P<0.05)。联合组胰岛β细胞胞质内粗面型内质网及核糖体较为丰富,可见较多分泌颗粒,核染色质分布均匀。模型组细胞膜不规则,染色质凝集,细胞质溶解,变性线粒体、膜不清,嵴致密;联合组细胞膜连续,核膜完整,常染色质较多且均匀,线粒体大小不等,嵴断裂呈空泡状。格列美脲组、联合组小鼠海马组织中GIP、GLP-1含量明显高于模型组(P<0.05),且联合组明显高于格列美脲组(P<0.05)。格列美脲组、联合组小鼠脑组织中MDA含量明显低于模型组、SOD活性高于模型组(P<0.05),联合组对MDA、SOD改善明显优于格列美脲组(P<0.05)。结论:黄芪多糖联合格列美脲可通过提高海马组织GIP、GLP-1含量及抗氧化能力,进而缓解糖尿病导致的认知功能障碍。Objective:To analyze the protective effect of astragalus polysaccharide combined with glimepiride on the cognitive dysfunction of diabetic mice induced by streptozotocin(STZ).Methods:Forty male ICR mice were selected and divided into normal control group,model group,glimepiride group,astragalus polysaccharide combined glimepiride group(combination group),all mice except the normal control group were given intraperitoneal injection STZ established a diabetic mouse model,and each administration group was given corresponding drugs by gavage for 6 consecutive weeks.Measure mouse body weight and fasting blood glucose changes;Morris water maze experiment to observe the spatial learning and memory ability of mice;transmission electron microscopy to observe the ultrastructure of pancreatic isletβcells and hippocampal neurons in each group of mice;to detect glucose-dependent insulin-promoting in the hippocampus of mice Polypeptide(GIP)and glucagon-like peptide-1(GLP-1)content;detection of superoxide dismutase(SOD)activity and malondialdehyde(MDA)content in mouse brain tissue.Results:After the administration,the weight of mice in the glimepiride group and the combination group was significantly higher than that of the model group,and the fasting blood glucose was significantly lower than that of the model group(P<0.05),and the weight of the mice in the combination group was significantly higher than that of the glimepiride,the fasting blood glucose in the urea group was significantly lower than that in the glimepiride group(P<0.05).From the 4th day,the escape latency of mice in the glimepiride group and the combination group was significantly shorter than that of the model group(P<0.05);the number of times the mice in the glimepiride group and the combination group crossed the platform was significantly higher than that in the model group(P<0.05),and the combination group was significantly higher than the glimepiride group(P<0.05).In the combination group,the cytoplasm of pancreaticβ-cells was rich in rough endoplasmic r

关 键 词：糖尿病 黄芪多糖 格列美脲 链脲佐菌素 认知功能障碍 小鼠 近交ICR 

分 类 号：R965[医药卫生—药理学]