目的 观察党参多糖对脂多糖（LPS）诱导的急性肺损伤（ALI）小鼠肺组织的保护作用，并探讨其作用机制。 方法 50只雄性昆明小鼠随机分为对照组，模型组，地塞米松组，党参多糖高剂量组（300 mg/kg）和党参多糖低剂量组（150 mg/kg）5个组。采用腹腔注射LPS法建立ALI小鼠模型。除对照组外，其余小鼠均根据分组给予灌胃给药。多参数肺功能检测系统检测小鼠0.3 s用力呼气量（FEV0.3）和用力肺活量（FVC）及其比值，苏木精-伊红（HE）染色法检测小鼠肺组织病理学变化，瑞氏-吉姆萨染色法检测小鼠肺泡灌洗液（BALF）中炎性细胞分类和计数，ELISA法检测BALF中IL-1β、IL-6、髓过氧化物酶（MPO）、TNF-α水平，Western blot法检测p-p38、p-IκB-α、p-p65蛋白表达量。 结果 与对照组比较，模型组小鼠出现了明显的肺病理损伤，FEV 0.3、FVC、FEV0.3/FVC检测值显著降低，肺组织湿质量/干质量（W/D）、BALF中性粒细胞、淋巴细胞、IL-1β、IL-6、MPO、TNF-α水平、p-p38 MAPK、p-IκB-α、p-p65蛋白表达显著增高（P < 0.05）。而党参多糖可缓解模型组小鼠上述变化。 结论 党参多糖可通过抑制MAPK/NF-κB通路，减轻急性肺损伤模型小鼠肺组织病理损伤，降低炎症因子水平，改善肺功能。

Objective To observe the protective effects of codonopsis pilosulae polysaccharide on lung tissues in mice with acute lung injury （ALI） induced by lipopolysaccharide （LPS） and its mechanism. Methods Fifty male Kunming mice were randomly divided into control group， model group， dexamethasone group， codonopsis polysaccharide high-dose group （300 mg/kg） and codonopsis polysaccharide low-dose group （150 mg/kg）. The ALI model was established by intraperitoneal injection of LPS. All mice were given gavage administration according to the grouping except for the control group. 0.3 s force expiratory volume （FEV 0.3） and force spirometry （FVC） and their ratios were measured using multiparametric lung function test system. The histopathology change of mouse lung was detected by hematoxylin-eosin （HE） staining， and the classification and count of inflammatory cells in alveolar lavage fluid （BALF） was detected by Richter-Giemsa staining. Levels of IL-1β， IL-6， MPO and TNF-α were measured by ELISA in BALF， and Western blot was used to detect the protein expression level of p-p38， p-IκB-α and p-p65. Results Compared with those in the control group， lung histopathological damage was more pronounced in the model mice， with significantly lower FEV 0.3， FVC， FEV0.3/FVC assay value， but significantly higher lung tissue wet mass/dry mass （W/D）， neutrophils， lymphocytes， IL-1β， IL-6， MPO， TNF-α， p-p38 MAPK， p-IκB-α， and p-p65 （P < 0.05）； while codonopsis pilosulae polysaccharide could significantly reverse these effects. Conclusion Codonopsis pilosulae polysaccharide plays a protective role against LPS-induced ALI via inhibiting MAPK/NF-κB pathway to reduce the pathological damage of lung tissue， and the level of inflammatory factors， thus to improve lung function in ALI model mice.