Augmenter of liver regeneration attenuates acute rejection after rat liver transplantation

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• 作者：Yong Chen ; Ph.D. ; M.D.^a ; ^b ; Shaoyong Liang ; Ph.D. ; M.D.^b ; Feiwu Long ; Ph.D. ; M.D.^b ; Jinzheng Li ; Ph.D. ; M.D.^b ; Jianping Gong ; Ph.D. ; M.D.^b ; ^{gongjianping11@126.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Augmenter of liver regeneration ; Kupffer cell ; Liver transplantation ; Immune regulation
• 刊名：The American Journal of Surgery
• 出版年：2016
• 出版时间：July 2016
• 年：2016
• 卷：212
• 期：1
• 页码：128-137
• 全文大小：3031 K

文摘

The role of augmenter of liver regeneration (ALR) on liver transplantation immune regulation remains unknown.

Methods

Male Lewis and Brown-Norway (BN) rats were assigned to allograft group (Lewis-to-BN liver transplantation), isograft group (BN-to-BN), and ALR group (Lewis-to-BN, ALR, 100 μg/kg/d, intramuscular injection postoperatively). Rats were sacrificed at indicated times for assessment of cytokines production, T-cell (TC) activation and apoptosis. Kupffer cells (KCs) and TCs were isolated from grafts to assess cytokine expression. Effect of ALR and KCs on TCs was monitored by co-culture of ³H-thymidine TCs.

Results

(1) Treatment with ALR significantly decreased interleukin-2 and interferon-γ expression, promoted TC apoptosis, and prolonged the survival of allografts; (2) KCs in ALR group and isograft group that had significantly increased interleukin-10 and decreased tumor necrosis factor-α expression were able to inhibit TC proliferation and induce their apoptosis relative to KCs in the allograft group; (3) ALR and KCs directly inhibited TC proliferation and activation and induced TC apoptosis.

Conclusions

ALR could inhibit TC proliferation and function both in vivo and in vitro and attenuate acute rejection after liver transplantation.