饮用酒和食用酒精暴露诱导小鼠肝脏组织的损伤效应

探究饮用酒和食用酒精暴露诱导小鼠肝脏组织损伤的损伤效应及可能的分子机制。将30只雄性C57BL/6 J小鼠随机分为对照组、饮用酒处理组和食用酒精处理组,每组10只,灌胃结束后,检测各组小鼠肝脏组织中氧化应激(ROS、MDA、SOD)、自噬反应(LC3B、Beclin-1)和细胞凋亡(Bax、Bcl-2、P53)等相关因子表达。结果显示,与对照组相比,饮用酒处理组的活性氧自由基ROS活性增加,过氧化氢酶MDA水平上调,超氧化物歧化酶SOD水平降低;自噬相关因子Beclin-1和LC3B的表达增加;同时,抗凋亡基因Bcl-2表达降低,促凋亡基因Bax表达增加,Bax/Bcl-2的比值上调,抑癌基因P53的表达呈上升趋势;食用酒精处理组呈现相同的变化,且趋势更明显。结果表明,饮用酒暴露可能通过刺激小鼠肝脏组织氧化应激的发生,进而引起细胞自噬和凋亡;与饮用酒相比,食用酒精对小鼠肝脏组织的损害效应更为明显,提示饮用酒中某些物质可能对小鼠肝脏组织起到一定的保护作用。

Alcohol Exposure Induced Toxic Effects and Molecular Mechanism in Mice Liver

To investigate the toxic effects and molecular mechanism of alcoholic drinks and edible alcohol exposure induced liver damage in mice,30 male C57BL/6 J mice were randomly divided into the control group,the alcoholic drinks exposure group and the edible alcohol exposure group,with 10 mice in each group.After gavage,the expression of oxidative stress(ROS,MDA,SOD),autophagy(Beclin-1,LC3B)and apoptosis(Bax,Bcl-2,P53)in the liver was determined.The results showed that,alcoholic drinks could significantly up-regulate ROS and MDA activity,decrease SOD level,accelerate Beclin-1,LC3B,Bax and P53 protein expression,reduce Bcl-2 level,and increase Bax/Bcl-2 ratio.The edible alcohol group showed the same change as the alcoholic drinks group,and the trend was even more obvious.In conclusion,alcohol exposure may induce autophagy and apoptosis via stimulate oxidative stress in mice liver;compared with alcoholic drinks,the damage effect of edible alcohol exposure was more obvious,suggesting that some substances in alcoholic drinks might have some protective effects on mice liver.