Abstract: Objective To investigate the effect and potential mechanism of alpinetin (ALPN) on bleomycin (BLM)-induced pulmonary fibrosis in mice. Methods The mice were randomly divided into control group, model group (intratracheally instilled BLM), low-dose (L-ALPN group) and high-dose ALPN groups (H-ALPN group) (10 mg/kg or 30 mg/kg ALPN daily, respectively) with 10 in each. Lung tissues were collected, and the alveolar structure and pathological morphology weremicroscopied by HE and Masson staining; mRNA and protein expressions of collagen Ⅰ, TGF-β1, E-cadherin, α-SMA, p-PERK, PERK, CHOP and GRP78 in lung tissue were detected by RT-qPCR, immunohistochemistry and Western blot, respectively. Results Compared with control group, the lung of the model group showed fibrotic changes, and the expression of collagenⅠ, TGF-β1, α-SMA, p-PERK/PERK, CHOP and GRP78 in lung tissue was significantly increased (P＜0.01). E-cadherin expression was significantly decreased (P＜0.01). Compared with model group, pulmonary fibrosis was significantly alleviated in low and high doses ALPN groups, the expression of collagen Ⅰ, TGF-β1, α-SMA, p-PERK/PERK, CHOP and GRP78 in lung tissue were significantly decreased (P＜0.05 or P＜0.01), and the expressionof E-cadherin was significantly increased (P＜0.05 or P＜0.01). Conclusions ALPN may alleviate BLM-induced pulmonary fibrosis, and this effect may be attributed to the inhibition of endoplasmic reticulum stress.

Key words: alpinetin, bleomycin, endoplasmic reticulum stress, pulmonary fibrosis