干扰素治疗肝纤维化机制的研究进展  

Therapeutic mechanism of interferon's anti-hepatic fibrosis action

作　　者：胡静[1] 李智伟[1] 

机构地区：[1]中国医科大学附属盛京医院感染科,辽宁省沈阳市110004

出　　处：《世界华人消化杂志》2007年第26期2809-2813,共5页World Chinese Journal of Digestology

摘　　要：肝纤维化是多种病因导致慢性肝病共有的病理改变,肝纤维化为一动态过程,属可逆性病变,但若进一步发展至肝硬化阶段,则不可逆,因此阻断抑制或逆转肝纤维化是治疗慢性肝病的一个十分重要的目标.干扰素(interferon,IFN)具有广泛的抗病毒、抗肿瘤和免疫调节作用.目前有许多研究认为干扰素(IFN)具有抗肝纤维化作用,并已在临床应用中取得一定效果,但其抗肝纤维化的确切机制尚不明了,有学者认为可能与其抗病毒,抑制肝星状细胞的活化增殖,促进肝星状细胞的凋亡,抑制细胞外基质(ECM)合成,促进细胞外基质降解等作用有关.Hepatic fibrosis is a common pathological change occurring in chronic liver disease which is induced by a variety of etiological factors. Hepatic fibrosis is a dynamic process, and a reversible pathological change. However, when it has progressed to hepatic cirrhosis, it is irreversible. Therefore, to block or reverse the course of hepatic fibrosis is a very significant target for the treatment of chronic liver disease. Interferon （IFN） has extensive functions, including anti-viral, anti-tumor and immunological roles. Recent research has reported that IFN possesses an antihepatic fibrosis function, with potential clinical application. However, the exact mechanism underlying its anti-hepatic fibrosis action remains unknown. Some scholars believe that this mechanism involves interferon＇s antiviral effects, the inhibition of hepatic stellate cell （HSC） activation, the promotion of HSC apoptosis, the inhibition of extracellular matrix （ECM） synthesis and the promotion of ECM degradation.

关 键 词：干扰素 肝纤维化 细胞外基质 肝星状细胞 

分 类 号：R575.2[医药卫生—消化系统]