甘草酸苷通过NF-κB通路影响小鼠急性肝损伤机制的研究

Study on the mechanism of SNMT on acute liver injury in mice by NF-κB signaling pathway

目的探讨甘草酸苷是否可通过调控核因子-κB（NF-κB）通路影响小鼠急性肝损伤。方法选取200只体质量29-30g昆明小鼠,分为4组,每组50只。第1组为对照组;第2组由四氯化碳（CCl4）诱导急性肝损伤;第3组在第2组的基础上注射复方甘草酸苷（SNMC）注射液;第4组在第3组的基础上加用NF-κB抑制剂（proDTC）。处理1、3、5d后,检测小鼠血清丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、总胆红素、清蛋白水平及凝血酶原时间（PT）,计算Child-Pugh评分并进行病理学观察。结果相较于第1组,CCL4处理后,AST、ALT、总胆红素、清蛋白表达水平,以及PT和Child-Pugh肝功评分均明显升高（P〈0.05）,表明已成功建立CCL4诱导急性肝损伤模型。同时给予小鼠SNMT后（CCL4＋SNMT）,各指标表达虽未回至正常水平,但随着处理时间的延长,表达水平逐渐降低（P〈0.05）。同时此效应可被NF-κB抑制剂proDTC逆转。结论SNMT可通过调节NF-κB通路降低小鼠急性肝损伤的严重程度。

Objective To explore whether glycyrrhizin has protective effect on acute liver injury in mice by NF-κB signaling pathway.Methods Totally 200 Kunming mice which the body weight were about 29-30 g were chose and divided into 4groups randomly,50 cases in each group.The first group was the control group;the second group was acute liver injury group induced by CCl4;the third group was injected with Stronger Neo-Minophagen C（SNMC）injection on the basis of second groups;the fourth group was treated with NF-κB inhibitor（proDTC）on the basis of the third group.After 1,3,5dtreatment,the serum expressing levels of ALT,AST,total bilirubin,albumin of mice and prothrombin time were detected,the Child-Pugh score was calculated,and the pathological observation was performed.Results The results showed that,compared to the first group,after CCl4 treatment,the expressing levels of AST,ALT,total bilirubin and albumin,the PT and Child Pugh score all were significantly increased（P0.05）,which indicated that the acute liver injury model induced by CCl4 was successfully established.After the treatment of SNMT（CCl4＋SNMT）in mice,although the level of each index did not return to normal level,with the extension of treatment time,the level of each index was also significantly reduced（P0.05）.At the same time,this effect could be reversed by NF-κB inhibitor proDTC.Conclusion SNMT plays a significantly protective role in acute liver injury via regulating NF-κB signaling pathway.