依达拉奉对乙醇致肝细胞损伤的保护作用  

Protective Effect of Edaravone on Hepatocyte Injury Induced by Ethanol

作　　者：刘永华[1] 夏晓虹[1] 唐彤丹[1] 付瑶[1] LIU Yong-hua;XIA Xiao-hong;TANG Tong-dan;FU Yao(Emergency Department of Internal Medicine,Dalian Central Hospital,Dalian,Liaoning Province,116033 China)

机构地区：[1]大连市中心医院急诊内科病房,辽宁大连116033

出　　处：《系统医学》2018年第17期20-23,共4页Systems Medicine

摘　　要：目的研究依达拉奉对酒精致肝细胞损伤的保护作用,并探讨其作用机制。方法 2016年3月—2017年10月,该院以MTT法测定细胞活力,筛选乙醇及依达拉奉浓度,倒置显微镜观察细胞形态,SOD、MDA测定细胞抗氧化及氧化水平, ELISA法检测细胞caspase3的表达,流式细胞术检测细胞凋亡,Western blot检测肝细胞TNF-α蛋白的表达。结果 125μmol/L依达拉奉与0.2 mol/L乙醇作用细胞24 h后,依达拉奉干预组细胞存活率为(81.53±0.69)%,高于乙醇模型组(73.99±1.89)%,差异有统计学意义(P<0.05)。依达拉奉组SOD含量为(16.33±2.06)U/mL较乙醇组(10.65±1.12)U/mL升高,依达拉奉组MDA含量为(2.31±0.33)nmol/mL,较乙醇组(3.68±0.39)nmol/mL下降,依达拉奉组Caspase3的表达(1.97±0.31)ng/mL,较乙醇组(2.89±0.35)ng/mL减少,差异均有统计学意义(P<0.05)。依达拉奉干预组细胞凋亡率为(10.32±0.89)%,明显低于乙醇模型组(15.68±1.07)%,差异有统计学意义(P<0.05)。依达拉奉组TNF-α蛋白水平(0.386±0.059)低于乙醇组(0.673±0.061),差异有统计学意义(P<0.05)。结论依达拉奉对酒精诱导体外肝细胞损伤具有保护作用,其机制可能与依达拉奉减轻氧化应激,抑制细胞凋亡有关。Objective To study the protective effect of edaravone on alcohol-induced hepatocyte injury and to explore its mechanism of action. Methods From March 2016 to October 2017, the cell viability was measured by MTT method. The concentration of ethanol and edaravone was screened. The morphology of the cells was observed by inverted microscope. The antioxidant and oxidative levels of cells were determined by SOD and MDA. The cells were detected by ELISA. The expression of caspase3 was detected by flow cytometry, and the expression of TNF-α protein in hepatocytes was detected by Western blot. Results After treated with 125 μmol/L edaravone and 0.2 mol/L ethanol for 24 h, the cell survival rate of edaravone intervention group was （81.53±0.69）%, which was higher than that of ethanol model group （73.99±1.89）%, with statistical significance （P〈0.05）. The SOD content of the edaravone group was （16.33±2.06） U/mL, higher than that of the ethanol group （10.65±1.12） U/mL, and the MDA content of the edaravone group was （2.31±0.33） nmol/mL, compared with the ethanol group of （3.68±0.39） nmol/mL, the expression of Caspase3 in the edaravone group was （1.97±0.31）ng/mL, which was significantly lower than that in the ethanol group （2.89±0.35） ng/mL（P〈0.05）. The apoptosis rate of edaravone intervention group was 10.32±0.89%, which was significantly lower than that of ethanol model group （15.68±1.07）%. The difference was statistically significant （P〈0.05）. The level of TNF-α protein in the edaravone group （0.386±0.059） was lower than that in the ethanol group （0.673±0.061）, and the difference was statistically significant （P〈0.05）. Conclusion Edaravone has a protective effect on alcohol-induced hepatocyte injury in vitro, and its mechanism may be related to the inhibition of oxidative stress and inhibition of apoptosis by edaravone.

关 键 词：依达拉奉 酒精性 肝细胞 凋亡 氧化应激 

分 类 号：R459[医药卫生—治疗学]