脂氧素对大鼠局灶性脑缺血/再灌注损伤的保护作用

目的 探讨脂氧素(lipoxin A_4,LXA_4)对大鼠局灶性脑缺血/再灌注损伤后炎症反应的影响.方法 雄性健康SD大鼠48只,体质量200～250 g,随机分为假手术组(S组)、缺血/再灌注组(I/R组),小剂量脂氧素A_4组(L组)和大剂量脂氧素A_4组(H组).建立大鼠局灶性脑缺血/再灌注模型,缺血2 h后拔出线栓实施再灌注.分别于再灌注后24 h观察大鼠神经功能缺损和脑组织病理学变化,测定脑梗死体积,脑组织髓过氧化物酶(MPO)活性和丙二醛(MDA)含量及白细胞介素-1β和肿瘤坏死因子-α的表达变化.结果 与I/R组比较,LXA4组缺血/再灌注24 h后神经功能改善,脑梗死体积缩小,MPO活性和MDA含量下降,IL-1β和TNF-α表达水平下调,脑组织病理学损伤减轻.结论 LXA4可能通过抑制缺血/再灌注所致脑组织损伤和促炎细胞因子的表达而起到脑保护作用.

Protective effects of lipoxin A4 on focal brain ischemia reperfusion injury in rats

Objective To investigagte whether LXA4 played protective role in preventing post-ischemic injury in the rat middle cerebral artery occlusion model. Methods Fourty-eight adult male Sprague-Dawley rats were divided randomly into four groups: sham-operated group, ischemia-reperfusion group (I/R group), low dose of LXA4 group (L group) and high dose of LXA4 group (H group). Rats were subjected to middle cerebral artery occlusion (MCAO). The neurological deficits, infarct volume and morphologic injury were assessed at 24 h. The myeloperxidase (MPO) activity and the lipid peroxidation levels were evaluated. The expressions of interleukin-β and tumor necrosis factor-α were studied by ELISA assay. Results LXA4 decreased MPO activity and malondialdehyde levels, reduced infarct fomation, and improved neurological recovery after 24 h. Also LXA4 down-regulated expression of IL-1β and TNF-α. Conclusion LXA4 may be a promising neuroprotective approach fo focal brain ischemia-reperfusion injury.