中文摘要：

目的探讨整合素CDllb在小鼠肝脏缺血再灌注损伤中的作用及其可能的机制。方法使用CD11b缺陷（CD11b-／-组）的C57BL／6小鼠和正常C57BL／6小鼠（wT组），制作小鼠70％肝脏缺血再灌注损伤模型：维持小鼠体温为37℃，暴露肝叶后用无损伤显微血管夹阻断肝脏左叶和中叶血流60min，然后恢复肝脏左叶和中叶血流，最后缝合腹部切口；另设假手术组（CDllb叫一Sham组和wTSham组）作为对照。再灌注后1、3、6、12、24和48h取血液，检测血清丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）水平；肝组织样本行HE染色和凋亡检测；Trizol试剂盒一步法提取肝组织细胞总RNA，检测肿瘤坏死因子a（TNF-a）和白细胞介素10（IL-10）的表达情况；提取枯否细胞，检测还原性辅酶Ⅱ（NADPH）氧化酶活性及活性氧的生成情况。结果CDllb-／-组小鼠术后ALT、AST升高程度显著低于WT组小鼠（P〈O．05）。肝组织HE染色显示CD11b-/-组小鼠肝细胞坏死、充血和肿胀程度明显轻于wT组小鼠（P〈0．05）；CDlIb-／-组缺血再灌注后3h肝细胞凋亡比例为（22．8±5．8）％，低于WT组的（66．6±10．2）％，差异有统计学意义（P〈O．05）。CDllb-/-组小鼠TNF-α表达低于wT组小鼠，而IL-10表达却高于wT组小鼠（P〈O．05）。CD11b-/-组小鼠的NADPH氧化酶活性及活性氧产生均低于wT小鼠（P〈0．05）。结论整合素CDllb可以调控炎症因子（TNF-α）和抗炎症因子（IL-10）的释放，增强枯否细胞NADPH氧化酶的活性，继而影响活性氧的生成，最终加重肝脏缺血再灌注损伤。

英文摘要：

Objective To investigate the role of integrin CDllb in liver ischemia/reperfusion （I/ R） injury and its possible mechanism. Method CD11b-/- and WT （C57BL/6） mice were used to establish a 70% liver warm I/R by clamping the left and median liver lobes for 60 min with vascular micro clamp at 37℃, then the clamp was removed and the abdominal incision was sutured. The blood plasma and liver samples were obtained at different time points （1, 3, 6, 12, 24 and 48 h） post- reperfusion to assess liver function and cellular injury. Serum ALT and AST levels were determined, and HE staining and TUNEL assay were performed to estimate the severity of liver damage. Tumor necrosis factor-α （TNF-α） and interleukin-10 （IL-10） were assayed by Reverse transcription polymerase chain reaction （RT-PCR）. Kupffer cells were isolated from the live, and the reduced form of nicotinamide-adenine dinucleotide phosphate （NADPH） oxidase activity and active oxygen species （ROS） production were assayed. Result CDllb-/- mice displayed a significantly preserved liver function as represented by lower alanine aminotransferase （ALT） and aspartic transaminase （AST） levels, less histological damage and apoptosis compared to WT mice. Furthermore, TNF-α was decreased and IL-10 mRNA expression was increased in CDllb-/- mice compared to WT mice. Finally, CDllb-/- mice showed decreased activity of NADPH oxidase and less ROS production. Conclusion Integrin CDll b may regulate the levels of inflammatory （TNF-α） and anti-inflammatory （IL-10） cytokines, enhance the activity of NADPH oxidase in Kupffer cells and enrich the production of ROS, which aggravate liver I/R injury.