目的 觀察注射用益氣復(fù)脈（凍干，YQFM）對(duì)脂多糖（LPS）誘導(dǎo)小鼠急性肺損傷（ALI）的保護(hù)作用。方法 C57雄性小鼠隨機(jī)分為對(duì)照組、模型組、注射用地塞米松磷酸鈉（DEX，5 mg/kg）組和YQFM低、中、高劑量（0.33、0.67、1.34 g/kg）組。YQFM和DEX均在氣管滴注LPS（5 mg/kg）前10 min經(jīng)尾iv給藥，24 h后，檢測(cè)肺濕干質(zhì)量比；制作肺組織切片進(jìn)行HE染色，觀察肺組織損傷及炎癥；收集支氣管肺泡灌洗液（BALF），分析BALF中的一氧化氮（NO）、丙二醛（MDA）、超氧化物岐化酶（SOD）、腫瘤壞死因子-α（TNF-α）、白細(xì)胞介素-1β（IL-1β）、總蛋白含量、中性粒細(xì)胞占比；制備肺組織勻漿，檢測(cè)髓過(guò)氧化物酶（MPO）活力，并用Western Blotting法檢測(cè)TLR4和MyD88蛋白表達(dá)水平。結(jié)果 與對(duì)照組比較，模型組肺組織損傷及炎癥反應(yīng)嚴(yán)重；小鼠肺濕干質(zhì)量比，BALF中的NO、MDA、TNF-α、IL-1β、總蛋白含量及中性粒細(xì)胞占比，肺組織中MPO活力、TLR4和MyD88蛋白表達(dá)均明顯升高，BALF中SOD含量明顯降低，差異均有統(tǒng)計(jì)學(xué)意義（P<0.05、0.01）。與模型組比較，YQFM組小鼠肺組織損傷及炎癥反應(yīng)緩解，BALF中NO、MDA、TNF-α、IL1-β、總蛋白含量及中性粒細(xì)胞占比，肺組織中MPO活力、TLR4和MyD88蛋白表達(dá)均明顯降低，SOD含量明顯升高，差異均有統(tǒng)計(jì)學(xué)意義（P<0.05、0.01）。結(jié)論 YQFM對(duì)氣管滴注LPS誘導(dǎo)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.

國(guó)家自然科學(xué)基金資金項(xiàng)目（81773971）