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作 者:顾文元[1] 李文静[2] 赵伟[3] 常柏[3] 张琳[3] 张宏[3]
机构地区:[1]天津中医药大学第二附属医院,天津300150 [2]聊城市第二人民医院 [3]天津医科大学代谢病医院内分泌研究所,卫生部激素与发育重点实验室
出 处:《山东医药》2014年第8期17-20,I0002,共5页Shandong Medical Journal
基 金:天津市卫生局科技基金项目(2010KZ89)
摘 要:目的观察艾塞那肽(EX)对糖尿病(DM)大鼠心肌组织Bcl-2、Bax表达的影响。方法高糖高脂饲料喂养联合尾静脉注射小剂量链脲佐菌素建立DM大鼠模型20只,随机分为DM组、EX组,EX组皮下注射EX 1.0nmol/(kg·d),设正常对照10只(N组)。12周后,应用实时定量PCR、Western blot法检测大鼠心肌组织中的Bcl-2、Bax。结果 EX组大鼠空腹血糖(FBG)、糖化血红蛋白(HbA1C)与DM组比较,P均>0.05。与N组比较,DM组大鼠心肌Bcl-2 mRNA和蛋白表达降低(P均<0.01),Bax mRNA和蛋白表达升高(P均<0.01),且Bcl-2与Bax mRNA和蛋白表达比值下降(P均<0.01);EX组较DM组大鼠心肌Bcl-2 mRNA和蛋白表达升高(P均<0.01),Bax mRNA和蛋白表达降低(P均<0.01),Bcl-2与Bax mRNA和蛋白表达比值增加(P均<0.01)。结论艾塞那肽可能通过上调DM大鼠心肌组织Bcl-2表达、下调Bax表达,从而抑制心肌细胞凋亡,延缓DM心肌病变的发生、发展。Objective To observe the effect of exenatide(EX) on the expression of Bcl-2 and Bax in the myocardial tissues of rats with diabetes mellitus (DM).Methods Thirty male Wistar rats were randomly divided into normal group (N),DM group and EX-treated group(EX group).Diabetes mellitus was induced by feeding the high-sugary and high-fat diet and intraperitoneally injecting of a low dose of streptozotocin.After establishment of diabetes models,EX (1.0 nmol ·kg-1 · d-1) was administered by subcutaneous injection for 12 weeks in the EX group.At termination,the expression levels of Bcl-2 and Bax,and the ratio of Bcl-2/Bax mRNA were determined by real-time quantitative PCR,and Western blot,respectively.Results No significant difference was found in FBG and HbA1c of EX and DM groups (all P > 0.05).Compared with the N group,the mRNA and protein expression of Bcl-2 and the ratio of Bcl-2/Bax were decreased in the DM group (P ≤ 0.01),but the mRNA and protein expression of Bax was increased (P ≤ 0.01).Both mRNA and protein expression of Bcl-2 and the ratio of Bcl-2/Bax were increased in the EX group as compared with the DM group (all P ≤0.01) and the mRNA and protein expression of Bax was decreased (P ≤ 0.01).Contusion Exenatide inhibits the myocardial apoptosis,delays the occurrence and development of DM myocardial lesions by up-regulating the expression of Bcl2 and down-regulating the expression of Bax in the myocardial tissue of DM rats.
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