This study investigated the molecular mechanisms underlying the involvement of the Notch signaling pathway and autophagy in the development of pulmonary fibrosis in pigeon breeder’s lung (PBL). Rats were divided into control (Ctrl), PBL model (M), M + D (Notch signaling inhibition), M + W (autophagy inhibition), and M + R (autophagy induction) groups. Lyophilized protein powder from pigeon shedding materials was used as an allergen to construct a fibrotic PBL rat model. The mechanism by which Notch signaling regulated autophagy in the pulmonary fibrosis of PBL was investigated by inhibiting the Notch pathway and interfering with autophagy. Pulmonary interstitial fibrosis was significantly greater in the M group and the M + W group than in the M + D and M + R groups. The expression of α-smooth muscle actin was significantly higher in the M, M + D, and M + W groups than in the Ctrl group (P < 0.05). The expression of the cell autophagy markers Beclin1 and LC3 was lower in the M, M + D, and M + W groups than in the Ctrl group (P < 0.05), whereas Beclin1 and LC3 expressions were higher in the M + D and M + R groups than in the M group. The levels of reactive oxygen species in serum and lung tissues were higher in the M, M + D, M + W, and M + R groups than in the Ctrl group (P < 0.05). The Notch signaling pathway is involved in the pathological process of pulmonary fibrosis in the rat model of PBL by regulating autophagy.
