论文部分内容阅读
目的探讨在小鼠全肝缺血-再灌注(I-R)前后肝组织内腺苷2A受体的动态表达趋势,以及与肝脏组织炎症反应的关系。方法分别检测缺血前、缺血20min、再灌注0、1、3、6、12、18、24h后肝脏A2AR蛋白表达和肿瘤坏死因子α(TNF-α)、巨噬细胞炎性蛋白2(MIP-2)、细胞间黏附分子(ICAM-1)含量以及组织髓过氧化物酶(MPO)活性的变化。结果A2AR表达于再灌注后12h达高峰,随后逐渐下降,再灌注24h降至正常以下水平。而TNF-α、MIP-2和ICAM-1含量于再灌注后表达逐渐增高,3～6h达到高峰,随后逐渐降低。MPO的活性趋势与炎性因子基本一致。结论I-R后组织炎症可能诱导了A2AR表达升高,从而抑制炎性因子的表达及组织炎性损伤。
Objective To investigate the dynamic expression of adenosine 2’-receptor in liver before and after liver ischemia-reperfusion (I-R) in mice and its relationship with the inflammatory reaction in liver. Methods The expression of A2AR and the expression of tumor necrosis factor alpha (TNF-α) and macrophage inflammatory protein 2 (TNF-α) in liver before and 20 min after ischemia, MIP-2), intercellular adhesion molecule (ICAM-1) content and myeloperoxidase (MPO) activity. Results The expression of A2AR peaked at 12h after reperfusion, then gradually decreased and then decreased to below normal level 24h after reperfusion. The expression of TNF-α, MIP-2 and ICAM-1 increased gradually after reperfusion and peaked at 3 ~ 6h, then decreased gradually. MPO activity trends and inflammatory factors are basically the same. Conclusion I-R tissue inflammation may induce A2AR expression increased, thereby inhibiting the expression of inflammatory cytokines and tissue inflammatory injury.