摘要目的 探讨细胞凋亡信号分子Fas及Caspase家族在肝泡球蚴病宿主中的表达及意义.方法 16例配对泡型包虫患者(AE)肝脏标本,16只雌性BALB/C小鼠.分析肝脏标本中肝细胞病理变化、凋亡及Fas、Caspase-3、Caspase-8和Caspase-9的表达.结果 AE患者病灶周围肝细胞水肿,汇管区周围纤维化,肝细胞造型坏死；病灶周围肝细胞发生显著凋亡[(74.0±15.0)％比(4.2±3.3)％],Fas[ (71.3±19.0)％比(5.2±1.6)％]、Caspase-3[ (39.4±18.3)％比(3.3±2.9)％]、Caspase-8[ (37.6±3.5)％比(4.0±1.8)％]和Caspase-9[ (24.7±13.8)％比(2.0±1.4)％]高表达(P＜0.05).泡球蚴感染小鼠病灶处可见囊泡,肝组织纤维化严重；肝细胞发生显著凋亡[(37.5±5.2)％比(13.9±2.7)％],Fas[ (48.3±6.2)％比(4.6±1.2)％]、Caspase-3[(29.7±6.3)％比(5.2±1.9)％]、Caspase-8[ (23.1±2.9)％比(3.5±1.4)％]和Caspase-9[( 16.7±3.2)％比(2.3±1.1)％]高表达(P＜0.05).结论 泡球蚴感染引起宿主肝细胞凋亡,提示Fas及Caspase家族介导的细胞凋亡信号通路可能参与了泡球蚴所致肝损伤进程.

abstractsObjective To investigate the expression of Fas and Caspases in the liver of Echinococcus multilocularis ( E multilocularis) infected hosts.Methods Sxiteen paired samples of alveolar echinococcosis (AE)-infected patients and 16 BALB/C mice were seleced.The pathological changes of the liver,apoptosis and the expression of Fas,Caspase-3,Caspase-8 and Caspase-9 were observed.Results In AEinfected patients,hepatocytes around the lesions displayed edema,fibrosis was seen around the bile duct and hepatocytes had spotty necrosis.Significant apoptosis was observed in the hepatocyes of AE-infected patients [ (74.0 ± 15.0)％ vs.(4.2 ±3.3)％ ] with high expression ofFas [ (71.3 ± 19.0)％ vs.(5.2 ±1.6)％],Caspase-8 [(37.6±3.5)％ vs.(4.0±1.8)％],Caspase-9 [(24.7±13.8)％ vs.(2.0± 1.4) ％ ] and Caspase-3 [ (39.4 ± 18.3 ) ％ vs.(3.3 ± 2.9) ％ ] (P ＜ 0.05 ).In the liver of E multilocularis-infected mice,multiple granulomas were formed and obvious fibrosis appeared around E multilocularis lesions.Significant apoptosis of hepatocytes was observed 9 ( 37.5 ± 5.2) ％ vs.( 13.9 ± 2.7 ) ％ ]with high expression of Fas [ (48.3 ± 6.2 ) ％ vs.(4.6 ± 1.2 ) ％ ],Caspase-3 [ ( 29.7 ± 6.3 ) ％ vs.(5.2±1.9)％],Caspase-8 [(23.1 ±2.9)％ vs.(3.5±1.4)％] andCaspase-9 [(16.7±3.2)％ vs.(2.3 ± 1.1 )％ ] (P ＜0.05).Conclusion E multilocularis infection can lead to apoptosis of hepatocytes in hosts,suggesting the involvement of Fas- and Caspases-mediated apoptotic pathway in E multilocularisinduced liver injury.