Acute progressive hypoxic respiratory failure caused by various predisposing factors is known as acute respiratory distress syndrome (ARDS). Although penehyclidine hydrochloride (PHC), an anticholinergic drug, is widely applied in clinical practice, the specific mechanisms underlying PHC in the treatment of ARDS are not completely understood. In the present study, BEAS‑2B cells were treated with 10 ng/ml lipopolysaccharide (LPS) to establish an ARDS cell model and a rat model of acute lung injury (ALI). The influences of PHC and/or autophagy inhibitor (3‑methyladenine (3‑MA)) on the morphology, autophagy, proliferation and apoptosis of cells and tissues were evaluated using hematoxylin and eosin staining, Cell Counting Kit‑8 assays, Hoechst staining, TUNEL staining, flow cytometry, immunofluorescence assays, ELISAs and scanning electron microscopy. The expression levels of apoptosis‑ and autophagy‑related proteins were measured via western blotting. The results indicated that PHC enhanced proliferation and autophagy, and decreased apoptosis and the inflammatory response in LPS‑induced BEAS‑2B cells and ALI model rats. In addition, 3‑MA reversed the effects of PHC on proliferation, inflammation, apoptosis and autophagy in LPS‑induced BEAS‑2B cells. Therefore, the present study suggested that PHC demonstrated a protective effect in LPS‑induced ARDS by regulating an autophagy‑related pathway.
Keywords: penehyclidine hydrochloride; autophagy; acute respiratory distress syndrome; lipopolysaccharide; apoptosis.