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目的观察二十二碳六烯酸(DHA)预防脂多糖(LPS)性小鼠急性肺损伤(ALI)的效果,探讨其抗氧化作用机制。方法雄性昆明种小鼠经灌胃给予DHA 250、500 mg/kg,连续10 d,然后经腹腔注射6 mg/kg脂多糖建立ALI模型;染毒16 h后,分别对各组动物肺组织进行病理学观察,支气管-肺泡灌洗液(BALF)和肺脏中氧化、抗氧化指标检测。结果脂多糖明显损伤肺组织氧化和抗氧化系统,DHA能明显改善脂多糖导致的肺脏病理学改变;给予250、500 mg/kg的DHA可分别使肺脏髓过氧化酶活性比脂多糖组降低12.2%和27.6%(P<0.05或P<0.01),丙二醛降低12.5%和25.5%(P<0.05或P<0.01);BALF和肺脏中超氧化物歧化酶活性分别升高13.2%和23.0%(P<0.05或P<0.01),19.9%和36.1%(P<0.01);谷胱甘肽过氧化物酶活性升高20.2%和33.1%(P<0.01);总抗氧化能力升高48.5%和102.4%(P<0.01)。结论 DHA对脂多糖导致的肺组织损伤具有预防作用,可能与其抗氧化功能相关。
Objective To observe the effect of docosahexaenoic acid (DHA) on the prevention of acute lung injury (ALI) in lipopolysaccharide (LPS) -induced mice, and to explore its anti-oxidative mechanism. Methods Male Kunming mice were intraperitoneally injected with DHA 250, 500 mg / kg for 10 days, and then intraperitoneally injected with 6 mg / kg lipopolysaccharide to establish ALI model. After 16 h of exposure, the lung tissues of each group were subjected to Pathological observation, bronchoalveolar lavage fluid (BALF) and lung oxidation, anti-oxidation index detection. Results Lipopolysaccharide obviously damaged lung tissue oxidation and anti-oxidant system. DHA significantly improved the pathological changes of lung caused by lipopolysaccharide. Administration of 250 and 500 mg / kg DHA reduced lung myeloperoxidase activity by 12.2 % And 27.6% respectively (P <0.05 or P <0.01), and MDA and MDA decreased by 12.5% and 25.5% (P <0.05 or P <0.01). The activities of superoxide dismutase in BALF and lung increased by 13.2% and 23.0% (P <0.05 or P <0.01), 19.9% and 36.1% respectively (P <0.01), glutathione peroxidase activity increased by 20.2% and 33.1% (P <0.01), and the total antioxidant capacity increased by 48.5% % And 102.4% (P <0.01). Conclusion DHA can prevent lung injury induced by lipopolysaccharide, which may be related to its anti-oxidative function.