中文摘要：

目的通过观察低中量饮酒后小鼠心功能、离体心脏抗缺血再灌注损伤能力和相关蛋白表达差异，探索低中量饮酒的心血管保护作用的其他可能机制。方法20只雄性成年C57BL／6小鼠随机分为对照组和实验组。对照组给予正常饮水，实验组给予低中量梯度乙醇[第1周为0．42mol／L（2．5％），第2周为0．84mol／L（5%），第3周为1．68mol／L（10％），第4～6周为3．03mol／L（18％）]。6周后行心脏超声检查，检测左心室舒张末期内径（LVEDD）、左心室收缩末期内径（LVESD）、左心室舒张末期前壁厚度（LVAWD）、左心室舒张末期后壁厚度（LVPWD）、射血分数（EF）和左心室短轴缩短率（FS）。两组随机各取4只小鼠制备离体缺血再灌注模型（缺血30min，再灌注45min），应用2，3，5氯化三苯基四氮唑（TTC）染色检测梗死面积。余下小鼠应用H-E染色和Masson染色分析其心肌细胞横截面积和胶原分布。应用Western印迹法检测TNF-α、Fas相关死亡域蛋白（FADD）、肿瘤抑制基因p53（p53）和4-羟基壬烯醛（4-HNE）蛋白表达情况。结果两组间小鼠的LVEDD、LVESD、LVAWD、LVPWD、EF、FS、心肌细胞横截面积和心肌胶原含量的差异均无统计学意义（P值均〉0．05）。对照组的心肌梗死程度显著高于实验组（P〈O．05）。对照组心肌组织中TNF-α、FADD、p53和4-HNE的蛋白相对表达量均显著高于实验组（P值均〈0．05）。结论小鼠基础状态下低中量饮酒可能通过抑制TNF-α／FADD／p53信号通路减少心肌细胞凋亡和毒性物质4-HNE蓄积来抵抗缺血再灌注损伤。

英文摘要：

Objective To investigate the effect of low-to-moderate alcohol consumption on the Cardiac function, resistance to ischemia/reperfusion （I/R） injury in vitro and the expression of related proteins in mice, then to reveal the underlying mechanisms of low-moderate-alcohol consumption-induced cardioprotection. Methods Twenty adult male C57BL/6 mice were randomly divided into control group and alcohol group. The mice in the control group fed with water. The mice in the alcohol group were fed with incremental V/V alcohol as follows; 0.42mol/L（2.5%）, 0.84 mol/L （5%） and 1.68 mol/L （10%） in week 1-3, 3.03 mol/L （18%） in the following 3 weeks. Cardiac function was measured by echocardiography 6 weeks after feeding, including left ventricular end-diastolic diameter （LVEDD）, left ventricular end-systolic diameter （LVESD）, left ventricular diastolic anterior wall （LVAWD）, left ventricular diastolic posterior wall （LVPWD）, ejection fraction （EF） and fractional shorting （FS）. Four mice were randomly selected from each group for the Langendorff I/R model （30 minutes ischemia followed by 40 minutes reperfusion and the infarct size was evaluated by TTC staining. Andthe heart tissues of other mice were cut and stained with hematoxylin and eosin （H-E） and Masson staining to measure the cross-sectional areas and collagen content. The expression of tumor necrosis faclor-alpha （TNF-α）, Fas-associating protein with a novel death domain （FADD）, tumor suppressor gene （p53） and 4-hydroxy-2-nonenal （4-HNE） were examined by Western blot. Results There were no significant differences in LVEDD, LVESD, LVAWD, LVPWD, EF, FS, cross-sectional areas or collagen content between the two groups （all P〈0.05）. The ratio of infarct size and the expression of TNF-α, FADD, p53 and 4-HNE in the control group were significantly higher than those in alcohol group （all P〈0.05）. Conclusion Low-to-moderate alcohol consumption attenuates I/R injury possibly by inhibiting TNF-α/FADD