血管紧张素1-7在骨骼肌细胞糖代谢中作用的研究  

Study of the effect of Ang-(1-7) on glucose metabolism in skeletal muscle cells

作　　者：刘畅[1] 信中[1] 曹曦[1] 杨芳远 杨金奎[1] 

机构地区：[1]首都医科大学附属北京同仁医院内分泌科,100730

出　　处：《中国糖尿病杂志》2017年第1期62-66,共5页Chinese Journal of Diabetes

基　　金：国家自然科学基金青年基金(81400824);首都医科大学基础-临床科研合作基金(13JL28);首都医科大学附属北京同仁医院科研基金(TRYY-KYJJ-2014-040)

摘　　要：目的研究血管紧张素1-7[Ang-(1-7)]在骨骼肌细胞糖代谢中的作用。方法原代提取C57小鼠成肌细胞,诱导分化为成熟细胞,分别予Ang-(1-7)及A779干预,采用非同位素法检测2-脱氧葡萄糖摄取率,氯化硝基四氮唑蓝(NBT)染色法检测细胞内活性氧簇(ROS)含量,RT-PCR检测氧化应激相关基因表达;用Ang-(1-7)干预糖尿病大鼠(OLETF),Western blot检测骨骼肌组织胰岛素信号通路蛋白表达。结果 Ang-(1-7)增加原代培养的骨骼肌细胞葡萄糖摄取和骨骼肌pIRS-1(tyr1179)、pAkt(ser473)的蛋白表达,降低骨骼肌细胞中ROS的产生和还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)亚基p22、NOX1的表达。结论 Ang-(1-7)可改善骨骼肌糖代谢,其作用机制可能与改善骨骼肌氧化应激有关。Objective To study the effect of Ang-（1-7）on the glucose metabolism in skeletal muscle cells. Methods Primary cultured skeletal muscle cells from C57 mice treated with Ang-（1-7）or A779 were used to study glucose uptake with non-isotopic method detecting 2 deoxyglucose uptake rate.Fully differentiated C2C12 cells treated with Ang-（1-7）or A779 were used to study the effects of ROS production.The expression of P22 and NOX1 was detected by RT-PCR;Western blot was used to study pIRS-1（tyr1179）and pAkt （ser473） in skeletal muscle cells of diabetic rats which were infused of Ang-（1-7）. Results Ang-（1-7）increased the glucose uptake in skeletal muscle cells.Ang-（1-7）reduced the production of ROS and the expression of NADPH subunits p22 and NOX1 in skeletal muscle cells.Ang-（1-7）increased the protein expression of pIRS-1（tyr1179）and pAkt （ser473） in skeletal muscle cells of diabetic rats. Conclusion Ang-（1-7）may be involved in improving glucose metabolism in skeletal muscle cells by preventing oxidative stress.

关 键 词：血管紧张素1-7 氧化应激 葡萄糖摄取 

分 类 号：R587.1[医药卫生—内分泌]