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目的：探讨气管内应用脂质体携载的前列腺素Ｅ１（ＬｉｐＰＧＥ１）对油酸致大鼠急性肺损伤的保护作用及其机制。方法：Ｗｉｓｔａｒ大鼠４０只，随机均分为５组：正常对照组、油酸致伤组、ＬｉｐＰＧＥ１组、游离前列腺素Ｅ１（ＦＰＧＥ１）组和空白脂质体（ＰＬｉｐ）组。观察肺系数、肺湿重／干重比、肺组织碱性磷酸酶（ＡＬＰ）、血管紧张素转换酶（ＡＣＥ）、髓过氧化酶（ＭＰＯ）的活性和丙二醛（ＭＤＡ）含量的变化。结果：与油酸损伤组比较，ＬｉｐＰＧＥ１组的肺系数、肺组织湿重／干重比与ＭＰＯ活性、ＭＤＡ水平明显降低，而ＡＬＰ与ＡＣＥ活性显著提高；ＬｉｐＰＧＥ１的作用显著优于ＦＰＧＥ１；ＰＬｉｐ无效。结论：经气管内给予ＬｉｐＰＧＥ１对油酸引起的大鼠急性肺损伤有良好的保护作用，其机制可能与抑制肺内中性粒细胞的聚集与抗氧自由基所造成的损伤有关。
Objective: To investigate the protective effect and mechanism of endobronchial liposomal prostaglandin E1 (LipPGE1) on acute lung injury induced by oleic acid in rats. Methods: Forty Wistar rats were randomly divided into five groups: normal control group, oleic acid injury group, LipPGE1 group, free prostaglandin E1 (FPGE1) group and blank liposome (PLip) group. The changes of lung coefficient, wet weight to weight ratio of lung, alkaline phosphatase (ALP), angiotensin converting enzyme (ACE), myeloperoxidase (MPO) and malondialdehyde (MDA) . Results: Compared with oleic acid injury group, the lung coefficient, the wet weight / dry weight ratio, the MPO activity and the MDA level in the LipPGE1 group were significantly decreased, while the ALP and ACE activities were significantly increased; the effect of LipPGE1 was significantly better than FPGE1; . CONCLUSIONS: Lipopolysaccharide (ET) administered orally in the endotracheal tube has a good protective effect against acute lung injury induced by oleic acid in rats. The mechanism may be related to inhibiting the accumulation of PMN and the damage caused by antioxidant free radicals.