中文摘要：

目的 研究组蛋白去乙酰化酶（HDACs）在酒精致小鼠肝细胞损伤中的表达情况。方法 以体外培养的小鼠正常肝细胞株AML12为研究对象,MTT法测定不同浓度和时间点酒精对AML12细胞的抑制作用;流式细胞术检测酒精对AML12细胞凋亡的影响;实时定量PCR法检测酒精致AML12细胞损伤中HDACs的mRNA表达水平。结果 酒精浓度100mmol/L刺激24h,AML12细胞的存活率为84%,可以明显抑制小鼠正常肝细胞AML12的增殖（P〈0.05）;酒精浓度100mmol/L刺激24h,AML12细胞的凋亡率为16%,可以增加AML12细胞的凋亡（P〈0.05）。在酒精致AML12细胞损伤中,HDAC1、2、3、4、5、6、7、8的mRNA表达水平均下降（P〈0.05）,HDAC9的mRNA表达水平上升（P〈0.05）,HDAC10的mRNA表达变化差异无统计学意义。结论 在酒精致肝细胞损伤中,HDACs的表达水平发生不同程度的变化,提示和HDACs相关的表观修饰可能参与酒精性肝损伤的发生发展。

英文摘要：

Objective To investigate the expression changes of histone deacetylases （HDACs） levels in alcohol-in- duced liver cell injury in mice. Methods Mice liver cell line （AML12） was used as the research object in vitro, to determine alcohol inhibitory effect on AML12 cells at different concentrations and time points by using MIT method; flow cytometry anlaysis was used to determine alcohol induced apoptosis effect on AML12 cells. Real-time quantitative PCR analysis was used to detect mRNA expression levels of HDACs in alcohol-induced liver cell injury model. Results Upon the stimulation of alcohol concentration at 100 mmol/L for 24 h, the survival rate of AML12 cell was 84% ,indicating its significant role in inhibiting the proliferation of liver cell line（ AML12 ） （P 〈 0. 05 ） ; furthermore, the apoptosis rate of AML12 cells was 16%, showing it could increase the AML12 cell apoptosis（P 〈 0. 05）. Binge alcohol exposure induced liver cell injury and eventually resulted in deregulation of hepatic HDACs mRNA expressions. It could be observed visually that HDAC1,2,3,4,5,6,7,8 mRNA expressions were signifi- cantly down-regulated and HDAC9 mRNA expression was up-regnlated （P 〈 0. 05 ）. However, there was no signifi- cant difference in HDAC10 mRNA expression than control. Conclusion In alcohol-induced liver cell injury model, alcohol consumption affects HDACs mRNA levels and therefore, we speculate that histone deacetylases-mediated epigenetic modifications may play an important role in the pathogenesis of alcohol-induced hepatic injury.