RESUMEN
Objective:To investigate the protective effect and mechanism of Baihe Gujin Tang on lipopolysaccharide induced acute lung injury (LPS-ALI). Method:KM mice were randomly divided into 5 groups:blank control group, model group, dexamethasone 0.002 g·kg-1 group, Baihe Gujin Tang (0.417, 1.25 g·kg-1) group. Except for the blank control group, the other groups were given LPS to induce the mouse ALI model. Except for the blank control group and the model group, the other groups were continuously given intragastric administration for 7 days on the 1st to 7th days before modeling. The lung tissue of the mice was taken 6 h after modeling, and the wet/dry mass ratio (W/D) of the left lung was measured. The serum levels of superoxide dismutase(SOD), malondialdehyde (MDA),reactive oxygen species (ROS)and nitric oxide (NO) were detected in the mice. Thepathological changes of the lung tissues were observed by hematoxylin-eosin(HE) staining. The expression levels of nuclear factor E2 related factor 2(Nrf2), Kelch-likeECH-associated protein 1 (Keap1), p62 and autophagy associated proteinsLC3Ⅱ proteins in the lung tissues were detected by Western blot. Result:Compared with the blank control group, the W/D of the model group was significantly increased (PPPP-1 group was significantly lower (P-1 group and dexamethasone group were able to significantly inhibited MDA levels in serum (PPPPPPConclusion:Baihe Gujin Tang has obvious protective effect on LPS-ALI mice, and its mechanism may be related to the regulation of Nrf2/Keap1/autophagy feedback loop.