Department of Neonatal Surgery, Nanjing Children's Hospital Affiliated to Nanjing Medical University, Nanjing, China.
J Surg Res. 2011 Jan;165(1):158-64. doi: 10.1016/j.jss.2009.05.038. Epub 2009 Jun 25.
Allograft inflammatory factor-1 (AIF-1) plays an important role in immune response and vasculopathy in allografts. The present study investigated activation of AIF-1 in warm and cold ischemia-reperfusion (IR) injury of rat liver, and the potential inhibitory effect of FK506.
We used warm IR injury, orthotopic transplantation, and allograft rejection models in this study. We assessed expression of AIF-1 mRNA and protein, as well as its inducers interferon-γ (IFN-γ) and interleukin-1β (IL-1β). The potential inhibitory effect of FK506 on AIF-1 in a rat macrophage cell line and in these three models was also assessed.
AIF-1 mRNA and protein, as well as its inducers IFN-γ and IL-1β, were significantly increased in the warm IR injury, orthotopic transplantation, and allograft rejection models. Real-time RT-PCR and Western blotting showed that pretreatment with low-dose FK506 partially inhibited AIF-1 activation as well as its inducers (IFN-γ and IL-1β) in these three models. Western blotting showed that IFN-γ and IL-1β activated AIF-1 in a macrophage cell line, but pretreatment with FK506 did not inhibit AIF-1 activation in vitro. Hematoxylin and eosin staining showed that edema and necrosis in the liver, as well as alanine aminotransferase (ALT) in serum, of these three groups was reduced after FK506 pretreatment.
AIF-1 was activated in warm and cold IR injury, and pretreatment with low-dose FK506 partly inhibited AIF-1 activation and reduced warm and cold IR injury.
同种异体炎症因子-1（AIF-1）在同种异体移植物的免疫反应和血管病变中发挥重要作用。本研究探讨了 AIF-1 在大鼠肝脏热缺血再灌注（IR）损伤和冷缺血再灌注损伤中的激活作用，以及 FK506 的潜在抑制作用。
本研究采用热 IR 损伤、原位移植和同种异体排斥模型。我们评估了 AIF-1 mRNA 和蛋白的表达，以及其诱导剂干扰素-γ（IFN-γ）和白细胞介素-1β（IL-1β）。还评估了 FK506 在大鼠巨噬细胞系和这三种模型中对 AIF-1 的潜在抑制作用。
AIF-1 mRNA 和蛋白及其诱导剂 IFN-γ和 IL-1β在热 IR 损伤、原位移植和同种异体排斥模型中均显著增加。实时 RT-PCR 和 Western blot 显示，低剂量 FK506 预处理部分抑制了这三种模型中 AIF-1 的激活及其诱导剂（IFN-γ和 IL-1β）。Western blot 显示 IFN-γ和 IL-1β在巨噬细胞系中激活了 AIF-1，但 FK506 预处理不能抑制体外的 AIF-1 激活。苏木精和伊红染色显示，FK506 预处理后，这三组的肝组织水肿和坏死以及血清丙氨酸氨基转移酶（ALT）均减少。
AIF-1 在热和冷 IR 损伤中被激活，低剂量 FK506 预处理部分抑制了 AIF-1 的激活，减轻了热和冷 IR 损伤。
