红没药醇对对乙酰氨基酚致小鼠急性肝损伤的保护作用

Protective Effect of Bisabololon on APAP-induced Acute Liver Injury

目的探讨红没药醇对对乙酰氨基酚(APAP)致小鼠急性肝损伤的保护作用及其可能机制。方法 40只小鼠随机分为对照组、模型组、谷胱甘肽组和红没药醇组。造模后,谷胱甘肽组和红没药醇组按照相应剂量给药,治疗2 d后取材。HE染色切片观察各组小鼠肝组织的病理组织学变化,Tunel染色切片观察各组小鼠肝细胞凋亡情况,测定各组小鼠血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)的活性以及肿瘤坏死因子(TNF-α)、白介素6(IL-6)的水平。结果与模型组比较,谷胱甘肽组、红没药醇组ALT、AST活性以及TNF-α、IL-6水平下降(P<0.05);红没药醇组ALT、AST活性以及TNF-α、IL-6的水平显著低于谷胱甘肽组(P<0.05);与模型组比较,谷胱甘肽组、红没药醇组黄色或棕黄色胞核有所减少,肝细胞凋亡数量减少(P<0.01);与谷胱甘肽组比较,红没药醇组黄色或棕黄色胞核减少,肝细胞凋亡数量减少(P<0.05)。结论红没药醇对APAP导致的急性肝损伤具有抗炎抗凋亡的保护作用。

Objective To explore the protective effect of Bisabololon on APAP-induced acute liv- er injury in mice and its underlying mechanism.Methods Mice were randomly divided into Con- trol group, Model group,Glutathione group,and Bisabolol group.After model establishment, the mice in Glutathione group and Bisabolol group were administered for 2 days.The HE staining was used to observe the histopathological changes of liver tissue in each group.The Tunel stai- ning was used to observe the hepatocyte apoptosis.The activity of ALT and AST and the levels of tumor necrosis factor （TNF-oL） and interleukin-6 （IL-6） were measured.Results Compared with the Model group, the local necrosis of liver tissue and inflammatory cell infiltration in the Bisabolol group were alleviated.The activities of ALT and AST and the levels of TNF-α and IL- 6in serum decreased significantly（P〈O.01）and the number of hepatocyte apoptosis decraeased （P〈O.05） .Conclusion Bisabololmay can protect against APAP-induced acute liverinjury of mice through inhibition of inflammation and apoptosis.