机构地区:[1]云南省第三人民医院内分泌科,昆明650032 [2]昆明医科大学生物化学与分子生物学系,昆明650500 [3]昆明医科大学第一附属医院糖尿病科,昆明650031 [4]昆明医科大学第一附属医院移植科,昆明650031 [5]昆明学院医学院生物化学教研室,昆明650500
出 处:《西南师范大学学报(自然科学版)》2017年第11期37-43,共7页Journal of Southwest China Normal University(Natural Science Edition)
基 金:国家自然科学基金项目(81360128);云南省应用基础研究基金项目(2013FD052;2015FB046);云南省教育厅研究基金项目(2012C006;2013C081)
摘 要:目的:研究EGCG(Epigallocatechin Gallate)是否抑制骨骼肌组织的TRB3(Tribbles Homologue 3)表达,激活PI3K/AKT信号通路,促进骨骼肌对葡萄糖的摄取和利用.方法:80只SD(Sprague Dawley)大鼠随机分为正常对照组(20只)、模型对照组(20只)、EGCG低剂量治疗组(20只)和EGCG高剂量治疗组(20只).模型对照组、EGCG低剂量治疗组和EGCG高剂量治疗组给予高糖高脂饮食6个月后,EGCG低剂量治疗组和EGCG高剂量治疗组分别给予EGCG治疗,治疗4周和8周分别处死各组大鼠各半,检测血清中葡萄糖、胰岛素含量并计算胰岛素抵抗指数;检测骨骼肌组织TRB3和AKT的表达及AKT的磷酸化程度.结果:模型组中葡萄糖、胰岛素和胰岛素抵抗指数(p<0.05),EGCG治疗4周和8周后,各指标均降低(p<0.05);模型组中AKT的mRNA和蛋白质在各组中无差异,但P-AKT(473)在模型组表达下调,治疗后表达上调,8周治疗较4周明显(p<0.05).模型组中TRB3的mRNA和蛋白质表达增加(p<0.05),治疗后TRB3表达的下调,8周治疗较4周明显(p<0.05);结论:EGCG可降低血糖,其机制可能与抑制TRB3的表达,增加AKT的磷酸化程度,激活PI3K/AKT信号通路,促进骨骼肌细胞对葡萄糖的摄取和利用,抑制胰岛素抵抗.This paper aims to the study on whether EGCG can activate PI3 K/AKT signal pathway by restraining the expression of TRB3 in muscle tissue so as to increase the uptake and utilization of glucose in muscle cell.80 SD rats were randomly divided into the control group(20),the model group(20),the lower EGCG treatment group(20),and the higher EGCG treatment group(20)respectively.Aftergiving the rats the sugar and fat diet in the model group,the lower EGCG treatment group and the higher EGCG treatment group for 6 months,those in the lower EGCG treatment group and the higher EGCG treatment group were treated with EGCG by anintragastric injection,and then half of each were sacrificed after 4 weeks and 8 weeks respectively with a purpose to examine the indicators(glucose insulin)in serum andinsulin resistance index,calculate the expressions of TRB3 and AKT and detect thephosphorylation of AKT in the muscle tissue.Compared with those in the control group,the glucose,insulin and insulin resistance index were higher in model group,and the indicators in the lower EGCG treatment group and higher EGCG treatment group were lower compared with those in the model group.The mRNA and protein expression of AKT in every group were not different.However,in the model group,phosphorylation of AKT was decreased and phosphorylation of AKT was increased after the treatment of EGCG and the effect had advantages in dose and time dependence.The mRNA and protein expression of TRB3 in the model group were increased compared those of the control group,the expression was decreased after the different contraction of EGCG treating for 4 weeks and 8 weeks and the lowering of TRB3 in EGCG treatment group after 8 weeks was obvious compared with that in the EGCG treatment group after 8 weeks.It is concluded that EGCG can alleviate the expression of TRB3 and inhibit phosphorylation of AKT,so as to activate the PI3 K/AKT signal pathway and increase the uptake and utilization of glucose in muscle tissue.
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