Objective: To explore the regulatory effect of astragaloside Ⅳ on autophagy and pyroptosis in mice lung tissue with idiopathic pulmonary fibrosis (IPF) and its mechanism

in order to provide new ideas for the study of astragalus' effect against lung fibrosis. Method: C57bl/6 mice induced by intratracheal instillation of bleomycin (BLM) were randomly divided into 4 groups:sham-operated group

model group

astragaloside Ⅳ group and dexamethasone group. astragaloside Ⅳ and dexamethasone groups were given respectively astragaloside Ⅳ (50 mg·kg-1) and dexamethasone (0.125 mg·kg-1) each day

while physiological saline was given in sham surgery and model groups each day. At the 14th day

lung tissues were collected for the analysis of the effect of astragaloside Ⅳ on morphology

collagen

autophagy and pyroptosis protein expression by hematoxylin-eosin (HE)

Masson

immunohistochemistry (IHC) and Western blot. Result: Astragaloside Ⅳ significantly inhibited the inflammatory reaction of lung tissues and down-regulated the expression of collagen (P<0.01). The results of IHC and Western blot showed that astragaloside Ⅳ significantly increased the expression of LC3Ⅱ/β-actin (P<0.05)

inhibited the accumulation of p62 (P<0.05)

and decreased the expression of Caspase-1 (P<0.01)

IL-1β (P<0.05) and IL-18 (P<0.05). Conclusion: Astragaloside Ⅳ group shows alleviationof pulmonary fibrosis. The mechanism may be related to the inhibition of pyroptosis and theincrease of autophagy. The study shows the therapeutic potential of Astragaloside Ⅳ in inhibiting pulmonary fibrosis.