摘要
瞄准：探索巨噬细胞的表示在在老鼠跟随肝 ischemia/reperfusion 损害 IRI 的 Kupffer 房间(KC ) 的煽动性的 protein-1alpha (MIP-1alpha ) 。方法：四十只男 SD 老鼠随机被划分成五个组。在老鼠肝的部分温暖的 ischemia/reperfusion 损害的一个模型被建立。KC 在灌注以后被孤立并且孵化一个小时，六个小时， 12 h，和 24 h。肿瘤坏死因素高山哈(TNF-alpha ) 并且在上层清液的 interleukin-1beta (IL-1beta ) 被 ELISA 测量。在 KC 的 MIP-1alpha 被细胞化学的免疫和 RT-PCR 检测。结果：没有或很少 MIP-1alpha 蛋白质和 mRNA 在控制组的 KC 被表示。它在 IRI 组的表达式在灌注以后有重要增加(P 【
0.05 ) ，它与控制组相反。结论：在 KC 后面的肝 ischemia/reperfusion 损害的 MIP-1alpha 基因的活跃行为被假定是为肝的 ischemia/reperfusion 损害的主要原因之一。
AIM： To explore the expression of macrophage inflammatory protein-1α （MIP-1α） in Kupffer cells （KCs） following liver ischemia/reperfusion injury IRI in rats. METHODS： Forty male SD rats were divided randomly into five groups. A model of partial warm ischemia/ reperfusion injury in the rat liver was established. KCs were isolated and incubated one hour, six hours, 12 h, and 24 h after the reperfusion. Tumor necrosis factor alpha （TNF-α） and interleukin-lbeta （IL-1β） in the supernatants were measured by ELISA. MIP-1α in KCs was detected by immunocytochemical and RT-PCR. RESULTS： No or few MIP-1α protein and mRNA were expressed in the KCs of the control group. Its expression in the IRI group had a significant increase after the reperfusion （P 〈 0.05）, which was contrary to the control group. CONCLUSION： The active behavior of the MIP-1α gene in KCs following liver ischemia/reperfusion injury is assumed to be one of the major causes for the hepatic ischemia/reperfusion injury.
