利拉鲁肽对高糖培养的H9c2心肌细胞氧化应激和内质网应激的影响

Effects of Liraglutide on Oxidative Stress and Endoplasmic Reticulum Stress of H9c2 Myocardial Cells Cultured in High Glucose

目的:探讨利拉鲁肽对高糖培养的H9c2心肌细胞氧化应激和内质网应激的影响。方法:在H9c2细胞的高糖培养液中加入利拉鲁肽(LIRA)、活性氧簇分子(ROS)清除药N-乙酰半胱氨酸(NAC)处理24 h,用流式细胞术检测细胞的ROS水平,用Western blot的方法检测H9c2细胞内质网应激标志蛋白葡萄糖调节蛋白78(GRP78)和C/EBP同源蛋白(CHOP)的表达水平。结果:与正常糖对照组比较,高糖组细胞内的ROS含量、GRP78和CHOP的蛋白表达水平显著上升(P<0.01)。与高糖组比较,利拉鲁肽显著抑制了细胞内的ROS产生(P<0.01),降低了GRP78和CHOP的蛋白表达水平(P<0.05)。结论:利拉鲁肽能抑制高糖培养的H9c2细胞的氧化应激和内质网应激水平。

Objective： To investigate the effects of liraglutide on high glucose induced oxidative stress and endoplasmic reticulum stress of H9 c2 myocardial cells. Methods： Liraglutide and N-scavenger N-acetylcysteine（ NAC,a reactive oxygen species（ ROS）scavenger） were added to the H9 c2 cells culture solution for 24 h. The ROS levels were detected by flow cytometry,and Western blot was used to detect the expression levels of glucose regulated protein 78（ GRP78） and C/EBP homologous protein（ CHOP）. GRP78 and CHOP were the endoplasmic reticulum stress protein markers. Results： Compared with the control group,the ROS,GRP78 and CHOP protein levels significantly increased in the high glucose group（ P〈0. 01）. Compared with the high glucose group,liraglutide significantly reduced the overproduction of ROS（ P 〈 0. 01）. Liraglutide also decreased the protein expression levels of GRP78 and CHOP（ P〈0. 05）. Conclusion： Liraglutide can inhibit high glucose induced oxidative stress and endoplasmic reticulum stress of H9 c2 cells.