脂氧素A4对大鼠肠缺血再灌注损伤的保护作用

目的观察脂氧素A4对大鼠肠缺血再灌注损伤（IR）的保护作用。方法择健康雄性SD大鼠30只，体重240～280g，采用抽签法随机分为3组，假手术组（C组）、肠IR组和脂氧素A4治疗组（L组），每组10只。除C组外，其他两组大鼠分离肠系膜上动脉（SMA）后，通过夹闭SMA复制大鼠肠IR模型，缺血60min，然后开放SMA，再灌注120min,L组于开放SMA同时静脉内给予脂氧素A40．1mg／kg，所有大鼠在试验过程中均以09％氯化钠注射液10ml·kg^-1·h^-1持续输注。观察肠IR后肠黏膜的损伤程度，测定肠组织丙二醛（MDA）、髓过氧化物酶（MPO）、二胺氧化酶（DAO）活性、肿瘤坏死因子α（TNF—α）含量。结果与IR组比较，L组肠黏膜损伤程度较轻，能够反映肠黏膜损伤程度的DAO活性在肠组织中明显下降，过度氧化应激指标MDA、MPO在肠组织中明显升高，肠组织中TNF—α含量明显下降（P〈0．05）。结论脂氧素A4对大鼠肠IR损伤具有良好的保护作用，这种保护作用与减轻肠IR损伤后肠组织的过氧化应激、减少肠组织内中性粒细胞的聚集，降低肠组织中TNF—α含量有关。

Protective effects of lipoxin A4 on the ischemia reperfusion injury of intestine in rats

Objective To investigate the protective effect of lipoxin A4 on the ischemia reperfusion injury of intestine in rats. Methods Male sprague dawley rats（30） weighing 240 to 280g were randomly divided into three groups（10 for each group）：sham operated group （C group,just separated the superior mesenterie artery and did not occlude it）,untreated ischemia reperfusion group （IR group, the superior mesenteric artery （SMA） was occluded SMA blood flow for 60min by 2 hours of reperfusion）, pretreatment with lipoxin A4 group （L group, the superior mesenteric artery （SMA） was occluded SMA blood flow for 60min by 2 hours of reperfusion ,the same as time, lipoxin An （0.1mg/kg） was given by vein）, all rats were given normal soudium by vein during the experiment.then the content of MDA and neutrophil count tumor factor-α （TNF-α）,the levels of MPO and DAO of intestine tissue were detected respectively.Histomorpholofy changes of intestine tissue were observed with microscope. Results Pretrcatment with lipoxin A4 was campared with IR,the levels of DAO of intestine tissue was decreased,the content of MDA and the levels of MPO of intestine tissue were increased, count neutrophil tumor factor- α （TNF-α）and the histomorpholofy changes of intestine tissue were diminished remarkably. Conclusion lipoxin A4 can protect intestine mucosa significantly from ischemia reperfusion injury in rats,the mechanism of protective effect of lipoxin A4 are related to diminishing the aggregation and activation of polymorphonuclear neutrophils（PMN） and inhibiting TNF- α.