Abstract:

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.

Key words: codonopsis pilosulae polysaccharide, lipopolysaccharide, acute lung injury, inflammatory factors, MAPK/NF-κB pathway