棕榈酸诱导H9C2心肌细胞脂毒性损伤模型的建立  

Establishment of a Model of Lipotoxic Injury Induced by Palmitic Acid in H9C2 Cardiomyocytes

作　　者：周宇 刘涛[1,2] 鲍翠玉 ZHOU Yu;LIU Tao;BAO Cui-yu(School of Pharmacy,Hubei University of Science and Technology,Xianning Hubei 437100,China)

机构地区：[1]湖北科技学院药学院,湖北咸宁437100 [2]湖北科技学院糖尿病心脑血管病变湖北省重点实验室

出　　处：《湖北科技学院学报（医学版）》2018年第2期102-105,185,共5页Journal of Hubei University of Science and Technology(Medical Sciences)

基　　金：国家自然科学基金资助项目(51703055);湖北省自然科学基金资助项目(2017CFB99;2015CFC773);湖北省教育厅科学研究计划项目(B201696);湖北科技学院糖尿病专项基金(2016-18XZ09;14ZX-02)

摘　　要：目的探讨棕榈酸(PA)对H9C2心肌细胞造成的影响,建立H9C2心肌细胞脂毒性损伤模型。方法不同浓度(0.025、0.05、0.1、0.2、0.4、0.8 mmol/L)PA刺激H9C2心肌细胞24h,用MTT比色法检测细胞增殖情况;选择浓度为0.4 mmol/L的PA刺激H9C2心肌细胞12、24、48h,用MTT比色法检测细胞增殖情况;不同浓度PA刺激H9C2心肌细胞24h后用ROS试剂盒检测细胞活性氧发生情况、用Tunel试剂盒检测细胞凋亡情况。结果 0.4mmol/L PA刺激H9C2心肌细胞24h时,细胞增殖水平明显被抑制。与control组相比,PA浓度为0.2mmol/L时,细胞ROS水平及Tunel凋亡水平均有所增加,另外,细胞出现轻微凋亡相关形态学改变;当0.4mmol/L PA刺激H9C2心肌细胞24h时,细胞ROS和Tunel水平均出现明显增加,细胞质与细胞核均发生明显的细胞凋亡现象。结论 PA浓度为0.4mmol/L刺激H9C2心肌细胞24h时即可建立起脂毒性心肌损伤模型。Objective To investigate the effect of palmitic acid(PA)on H9C2 cardiomyocytes and to establish a model of lipotoxic injury in H9C2 cardiomyocytes.Methods H9C2 cardiomyocytes were stimulated with different concentrations of PA(0.025,0.05,0.1,0.2,0.4 and 0.8mmol/L)for different time,and the cell viability was detected by MTT assay.The occurrence of reactive oxygen species in cells was detected with ROS kit,and the cell apoptosis was detected with Tunel kit.Results The cell viability of H9C2 was significantly decreased after stimulation with palmitic acid at the concentration of 0.4mmol/L for 24h.Compared with the control group,the ROS level in H9C2 cardiomyocytes and the number of apoptotic cells.were increased after treatment with 0.2 mmol/L PA for 24 h,and the effects were more obvious with 0.4 mmol/L PA stimulation.Conclusion The model of lipidtoxic cardiomyocyte injury can establish by palmitic acid at the concentration of 0.4mmol/L for 24 h in H9C2 cell line.

关 键 词：糖尿病心肌损伤 棕榈酸 高脂 H9C2心肌细胞 

分 类 号：R961[医药卫生—药理学]