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目的研究依达拉奉影响肝脏缺血再灌注过程中TNF-α的表达情况,探讨依达拉奉对肝脏缺血再灌注损伤的逆转作用。方法将80只Wistar大鼠编号,根据计算机产生随机数字,前40为一组,后40为一组,分为实验组和对照组2组,建立常温下部分肝缺血再灌注损伤动物模型。在肝脏缺血再灌注损伤开始前1 h和开始时对实验组大鼠给予依达拉奉注射液10 ml,对照组则给予同等容量的生理盐水。分别于再灌注后0、1、2及4 h测定肝脏脂质过氧化物酶(LPO)和肝脏谷草转氨酶(AST)浓度;应用RT-PCR法检测肝组织TNF-αmRNA含量,并测定肝组织和血清中TNF-α水平;应用TUNEL染色法检测缺血肝组织的细胞凋亡情况。结果再灌注后1、2及4 h,实验组大鼠肝脏LPO及AST浓度均明显低于对照组(P<0.001);实验组再灌注后1 h时肝组织TNF-αmRNA表达量、肝组织和血清TNF-α含量均明显升高且达峰值,但均明显低于对照组(P<0.05);再灌注后各时相实验组肝细胞凋亡率明显升高,但均明显低于对照组(P<0.05)。结论依达拉奉能抑制氧化应激反应,从而降低肝缺血再灌注损伤;并显著减少炎性细胞因子TNF-α的产生,抑制炎性反应的发生,减少肝细胞的凋亡。
Objective To investigate the effect of edaravone on the expression of TNF-α during hepatic ischemia-reperfusion in rats and to explore the reversal effect of edaravone on hepatic ischemia-reperfusion injury. Methods Eighty Wistar rats were numbered and random numbers were generated according to the computer. The first 40 groups were divided into two groups, experimental group and control group. The animal model of partial hepatic ischemia-reperfusion injury was established at room temperature. Rats in the experimental group were given 10 mg Edaravone injection 1 h before and at the beginning of liver ischemia-reperfusion injury, while the control group received the same volume of saline. The levels of hepatic LPO and AST were measured at 0, 1, 2 and 4 h after reperfusion. The levels of TNF-α mRNA in liver tissue were determined by RT-PCR, And serum TNF-α levels; TUNEL staining was used to detect the apoptosis of ischemic liver tissue. Results At 1, 2 and 4 h after reperfusion, the levels of LPO and AST in the liver of the experimental group were significantly lower than those of the control group (P <0.001). At 1 h after reperfusion, the expression of TNF-α mRNA, (P <0.05). The apoptotic rate of hepatocytes in each experimental group after reperfusion was significantly higher than that of the control group Group (P <0.05). Conclusion Edaravone can inhibit oxidative stress and reduce hepatic ischemia-reperfusion injury. It also significantly reduces the production of inflammatory cytokines TNF-α, inhibits the inflammatory reaction and reduces the apoptosis of hepatocytes.