莱菔硫烷对高脂环境下心肌细胞保护作用  

Sulforaphane prevents palmitic acid-induced mitochondrial impairments of cardiomyocyte in vitro

作　　者：胡丽贞[1] 李雅杰[1] 薛宏凤[1] 王舒然[1] 

机构地区：[1]哈尔滨医科大学公共卫生学院营养与食品卫生教研室,黑龙江哈尔滨150086

出　　处：《中国公共卫生》2013年第10期1466-1469,共4页Chinese Journal of Public Health

基　　金：国家自然科学基金(81072297)

摘　　要：目的探讨莱菔硫烷对暴露高脂环境下H9c2心肌细胞保护作用。方法用350μmol/L棕榈酸作用于H9c2心肌细胞24 h建立细胞高脂损伤模型,用台盼蓝染色法检测不同剂量(1、5、7.5、10μmol/L)莱菔硫烷预处理24 h和5μmol/L莱菔硫烷预处理不同时间(12、24、36、48 h)后的细胞存活率,用荧光探针法检测活性氧(ROS)和细胞线粒体膜电位(MMP),用噻唑兰法检测线粒体琥珀酸脱氢酶(SDH)活性,用透射电子显微镜观察线粒体结构和形态改变,用逆转录-聚合酶链反应(RT-PCR)检测核呼吸因子1、2(NRF1、NRF2)mRNA表达水平。结果与对照组比较,模型组细胞存活率[(38.04±12.69)%]下降(P<0.05),莱菔硫烷(5μmol/L、24 h)预处理组细胞存活率[(69.37±6.35)%]明显上升(P<0.05);莱菔硫烷组ROS水平[(86.27±1.44)%]低于模型组[(124.72±11.54)%],差异有统计学意义(P<0.05);与模型组比较,莱菔硫烷组MMP、SDH活性[(37.88±6.92)%、(66.59±6.92)%]和NRF1、NRF2 mRNA表达水平[(61.72±11.58)%、(131.16±14.52)%]明显升高(P<0.05);莱菔硫烷预处理能明显减轻高脂诱导的细胞线粒体固缩,增加线粒体数量。结论莱菔硫烷能减轻高脂对心肌细胞线粒体损伤,保护暴露于高脂环境下的心肌细胞。Objective To investigate the protective effect of sulforaphane（SFN）on H9c2 myocardial cells treated with high fat.Methods H9c2 cells were cultured in vitro,and were treated with 350 μmol/L palmitic acid for 24 hours to set up cellinjury model.The model cells were pretreated with different dose of SFN（1,5,7.5,and 10 μmoll/L）for 24 hours and was pretreated by 5 μmol/L SFN for different time（12,24,36,and 48 hours）,then the cellular viabilities were detected with trypan blue staining.Fluorescent probes were used to determinate reactive oxygen species（ROS）and mitochondrial membrane potential（MMP）.Thiazolyl blue staining was used to detect mitochondrial succinic dehydrogenase（SDH）activity.Mitochondrial morphous was observed with electron microscope.The mRNA expression levels of nuclear respiratory factor 1 and 2（NRF1,NRF2）were detected with reverse transcription polymerase chain reaction（RT-PCR）.Results Compared to the control group,the cellular viability of cellinjury model group（38.04＆plusmn;12.69%）decreased（P〈0.05）,while SFN（5 μmol/L,24 hours）of pretreated group（69.37＆plusmn;6.35%）wase significantly increased（P〈0.05）.The ROS production of SFN group（86.27＆plusmn;1.44%）was significantly decreased compared to that of cellinjury model group（124.72＆plusmn;11.54 %）（P〈0.05）.The MMP,SDH activity（37.88＆plusmn;6.92 %,66.59＆plusmn;6.92%）and the mRNA expression levels of NRF1and NRF2（61.72＆plusmn;11.58% and 131.16＆plusmn;14.52%）of SFN group were significantly increased compared to cellinjury model group（P〈0.05）.SFN pretreatment alleviated mitochondrial pyknosis and mitochondrial quantity reduction.Conclusion Sulforaphane can reduce mitochondrial damage induced by high fat,therefore protect myocardial cells exposed to a high-fat environment.

关 键 词：莱菔硫烷 肥胖 心肌细胞 棕榈酸 线粒体 

分 类 号：R151.41[医药卫生—营养与食品卫生学]