脂氧素对大鼠局灶性脑缺血／再灌注损伤的保护作用

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

目的探讨脂氧素（lipoxin A4，LXA4）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200～250g，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A4组（L组）和大剂量脂氧素A4组（H组）。建立大鼠局灶性脑缺血／再灌注模型，缺血2h后拔出线栓实施再灌注。分别于再灌注后24h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-Iβ和肿瘤坏死因子-α的表达变化。结果与I／R组比较，LXA。组缺血／再灌注24h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。

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 - reper- fusion 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 vol- ume 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 ischemiareperfusion injury.