目的 观察注射用益气复脉（冻干，YQFM）对脂多糖（LPS）诱导小鼠急性肺损伤（ALI）的保护作用。方法 C57雄性小鼠随机分为对照组、模型组、注射用地塞米松磷酸钠（DEX，5 mg/kg）组和YQFM低、中、高剂量（0.33、0.67、1.34 g/kg）组。YQFM和DEX均在气管滴注LPS（5 mg/kg）前10 min经尾iv给药，24 h后，检测肺湿干质量比；制作肺组织切片进行HE染色，观察肺组织损伤及炎症；收集支气管肺泡灌洗液（BALF），分析BALF中的一氧化氮（NO）、丙二醛（MDA）、超氧化物岐化酶（SOD）、肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、总蛋白含量、中性粒细胞占比；制备肺组织匀浆，检测髓过氧化物酶（MPO）活力，并用Western Blotting法检测TLR4和MyD88蛋白表达水平。结果 与对照组比较，模型组肺组织损伤及炎症反应严重；小鼠肺湿干质量比，BALF中的NO、MDA、TNF-α、IL-1β、总蛋白含量及中性粒细胞占比，肺组织中MPO活力、TLR4和MyD88蛋白表达均明显升高，BALF中SOD含量明显降低，差异均有统计学意义（P<0.05、0.01）。与模型组比较，YQFM组小鼠肺组织损伤及炎症反应缓解，BALF中NO、MDA、TNF-α、IL1-β、总蛋白含量及中性粒细胞占比，肺组织中MPO活力、TLR4和MyD88蛋白表达均明显降低，SOD含量明显升高，差异均有统计学意义（P<0.05、0.01）。结论 YQFM对气管滴注LPS诱导小鼠ALI具有一定的防治作用。
Objective To observe the protective effect of YQFM injection on lipopolysaccharide (LPS) -induced acute lung injury (ALI) in mice. Methods C57 mice were randomly divided into control group, LPS group, YQFM low, medium, high dose (0.33, 0.67 and 1.34 g/kg) groups, and dexamethasone (DEX, 5 mg/kg) group. YQFM and DEX were tail vein injected 10 min before tracheal instillation of LPS (5 mg/kg). After 24 h, lung wet/dry weight ratio was observed, and the pulmonary tissue slices were stained with HE to observe the injury and inflammation of lung tissue. The levels of NO, malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor-α (TNF-α), interleukin -1β (IL-1β), total protein content, and neutrophil proportion were examined to collect the bronchoalveolar lavage fluid (BALF). The lung tissue homogenate was prepared, the myeloperoxidase (MPO) activity was detected, and the expression of TLR4 and MyD88 protein was detected by Western Blotting. Results Compared with control group, the lung tissue injury and inflammatory response were serious in model group, and the content of NO, MDA, TNF-α, IL1-β, total protein and the percentage of neutrophils, the activity of MPO, and the expression of TLR4 and MyD88 in BALF in model group were all increased significantly, and the content of SOD was decreased significantly (P < 0.05 and 0.01). Compared with model group, pulmonary tissue injury and inflammation were relieved, the contents of NO, MDA, TNF-α, IL1-β and total protein, the percentage of neutrophils, the activity of MPO, and the expressions of TLR4 and MyD88 in BALF were all decreased, and the content of SOD was increased in YQFM groups, the differences were statistically significant (P < 0.05). Conclusion YQFM has a certain prevention effect on LPS-induced acute lung injury in mice.