中文摘要：

瞄准：在老鼠在长期的肝 allograft 机能障碍上调查锌手指蛋白质 A20 的效果。方法：到路易斯老鼠的从 DA 老鼠的 Allogeneic 肝移植被执行。长期的肝 allograft 机能障碍被在手术后的白天(邮政部门) 管理低剂量的 tacrolimus 在老鼠导致 5。A20 的肝的 overexpression 被调停的基因转移静脉内地管理了的 recombinant 侵入人体气管粘膜的病菌(rAd ) 完成从邮政部门 10 开始的每 10 d。接受者老鼠被注射与生理盐， rAdEasy-A20 (1

英文摘要：

AIM： To investigate the effect of zinc finger protein A20 on chronic liver allograft dysfunction in rats. METHODS： AIIogeneic liver transplantation from DA rats to Lewis rats was performed. Chronic liver allograft dysfunction was induced in the rats by administering low-dose tacrolimus at postoperative day （POD） 5. Hepatic overexpression of A20 was achieved by recom- binant adenovirus （rAd.）-mediated gene transfer ad- ministered intravenously every 10 d starting from POD 10. The recipient rats were injected with physiologi- cal saline, rAdEasy-A20 （1 × 109 pfu/30 g weight） or rAdEasy （1 × 109 pfu/30 g weight） every 10 d through the tail vein for 3 mo starting from POD 10. Liver tissue samples were harvested on POD 30 and POD 60. RESULTS： Liver-transplanted rats treated with only tacrolimus showed chronic allograft dysfunction with severe hepatic fibrosis. A20 overexpression ameliorated the effects on liver function, attenuated liver allograft fibrosis and prolonged the survival of the recipient rats. Treatment with A20 suppressed hepatic protein pro- duction of tumor growth factor （TGF）-β1, interleukin- 113, caspase-8, CD40, CD40L, intercellular adhesion molecule-i, vascular cell adhesion molecule-1 and E-selectin. A20 treatment suppressed liver cell apopto- sis and inhibited nuclear factor-KB activation of Kupffer cells （KCs）, liver sinusoidal endothelial cells （LSECs） and hepatic stellate cells （HSCs）, and it subsequently decreased cytokine mRNA expression in KCs and LSECs and reduced the production of TGF-β1 in HSCs. CONCLUSION： A20 might prevent chronic liver allogra- ft dysfunction by re-establishing functional homeostasis of KCs, LSECs and HSCs.