Maiwei Yangfei decoction prevents bleomycin‑induced pulmonary fibrosis in mice

Maiwei Yangfei (MWYF) is a compound Chinese herb that is safe and effective in the clinical setting in patients with pulmonary fibrosis (PF). The aim of the present study was to assess the role of a (MWYF) decoction in a bleomycin (BLM)-induced PF mouse model and to investigate the underlying functional mechanism. Chemical components within the MWYF decoction were analysed using liquid chromatography-mass spectrometry. A total of 50 C57BL/6 mice were randomly assigned to one of the following five groups with 10 mice per group: Control, model, low dose MWYF (20 g/kg), medium dose MWYF (40 g/kg) and high dose MWYF (60 g/kg). A mouse PF model was established by the tracheal instillation of BLM (5 mg/kg) prior to MWYF treatment, except for mice in the control group. After 21 days of treatment with MWYF, the mice were sacrificed and the body weights were recorded. In addition, pulmonary tissues and bronchial alveolar lavage fluid were collected. TNF-α, IL-6, IL-17, hydroxyproline, pyridinoline and collagen I levels were determined using ELISA. Vimentin, α-smooth muscle actin (α-SMA), fibronectin, TGF-β1, Smad3, TNF-α, IL-6, IL-17, collagen I and collagen III were determined using western blotting. Vimentin and α-SMA levels were also determined using immunofluorescence analysis. Collagens I and III were detected using immunohistochemical analysis and TGF-β1 and Smad3 levels were determined using reverse transcription-quantitative PCR. Following treatment with MWYF decoction, the body weight of the mice in the PF group increased, the degree of pulmonary alveolitis and PF was reduced, collagen levels were reduced and the expression levels of α-SMA, vimentin and fibronectin were decreased. Although both protein and mRNA expression levels of TGF-β1 and Smad3 were reduced, they remained higher than those observed in the control group. To conclude, MWYF decoction delayed the development of BLM-induced PF in mice, where the functional mechanism was likely associated with the TGF-β1/Smad3 signalling pathway.

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