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作 者:刘行海[1] 徐策 买文丽[1] 郑倩[1] 刘华[1] 刘红[1] LIU Xing-hai;XU Ce;MAI Wen-li;ZHENG Qian;LIU Hua;LIU Hong(Department of Physiology,North Sichuan Medical College,Nanchong 637000,Sichuan,China)
机构地区:[1]川北医学院生理学教研室,四川南充637000
出 处:《川北医学院学报》2021年第1期14-16,共3页Journal of North Sichuan Medical College
基 金:四川省南充市市校合作科研项目(18SXHZ0297);四川省教育厅重点项目(17ZA0167)。
摘 要:目的:研究表没食子儿茶素没食子酸酯(EGCG)对2型糖尿病(T2DM)大鼠认知功能的影响及其机制研究。方法:30只大鼠中随机选择8只作为对照组,另22只采用高脂饮食联合链脲佐菌素复制T2DM,将造模成功的17只大鼠随机分成模型组(n=9)和EGCG组(n=8)。EGCG组给予EGCG灌胃,剂量为40 mg/kg,1次/d,对照组和模型组每次灌胃等体积生理盐水,连续4周。采用Morris水迷宫法评价大鼠认知功能,测定大鼠空腹血糖(FBG)、空腹血清胰岛素(FINS)水平并计算胰岛素敏感指数(ISI),ELISA检测大鼠海马组织肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)含量,Western blotting检测海马组织核因子-κB p65(NF-κB p65)蛋白表达。结果:与对照组比较,模型组大鼠逃避潜伏期增加,穿越平台次数减少(P<0.05);FBG、FINS升高,ISI降低(P<0.05);海马TNF-α和IL-6含量升高,NF-κB p65蛋白表达增加(P<0.05)。与模型组比较,EGCG组逃避潜伏期减少,跨越原平台位置次数增加(P<0.05);FBG、FINS降低,ISI升高(P<0.05);海马TNF-α和IL-6含量降低,NF-κB p65蛋白表达减少(P<0.05)。结论:EGCG对T2DM大鼠认知功能减退有改善作用,其机制可能与抑制TNF-α,IL-6及NF-κB p65蛋白表达,从而减轻海马炎症反应有关。Objective:To study the effect of epigallocatechin gallate(EGCG)on cognitive function of type 2 diabetes mellitus(T2DM)rats and its mechanism.Methods:8 of the 30 rats were randomly selected as the control group,and the other 22 rats were induced by hight-fat diet and streptozotocin to replicate T2DM.17 successful rats were randomly divided into model group(n=9)and EGCG group(n=8).EGCG group was given EGCG by gavage,the dose was 40 mg/kg,once a day,while the control group and model group were given the same volume of normal saline every time for 4 weeks.The cognitive function of rat was evaluated by the morris water maze test.Fasting blood glucose(FBG),fasting serum insulin(FINS)levels were measured and insulin sensitivity index(ISI)was calculated.The contents of tumor nerosis factor-α(TNF-α)and interlukin-6(IL-6)in hippocampus were detected by enzyme-linked immunosrbent assay(ELISA)and The NF-κB p65 protein expression in hippocampus was detected by western blotting.Results:Compared with control group,the escape latency increased while the number of crossing platform decreased in model group(P<0.05),FBG and FINS increased and ISI decreased in model group(P<0.05).The expression of NF-κB p65,TNF-αand IL-6 increased in hippocampus in model group(P<0.05).Compared with model group,the escape latency decreased while the number of crossing platform increased in EGCG group(P<0.05),FBG,FINS decreased and ISI increased in EGCG group(P<0.05).The expression of NF-κB p65,TNF-αand IL-6 decreased in hippocampus in EGCG group(P<0.05).Conclusion:EGCG can improve the cognitive decline in T2DM rat and its mechanism may be related to reducing the inflammatory response in hippocampus by inhibiting TNF-α,IL-6 and NF-κB p65 protein expression.
关 键 词:表没食子儿茶素没食子酸酯 2型糖尿病大鼠 认知障碍 海马 炎症
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