Licochalcone A in Inhibiting Bleomycin-induced Pulmonary Fibrosis Through TGF-β/Smad Pathway / 中国实验方剂学杂志

ABSTRACT

Objective: To explore the therapeutic effect of licochalcone A (Lico A) on pulmonary fibrosis (PF). Method: Thirty mice were divided into five group, namely sham, model, Lico A (15, 30 mg·kg-1) and pirfenidone (300 mg·kg-1) groups. All of the groups except for sham group were intratracheally given bleomycin (BLM, 5 mg·kg-1). The sham group was given normal saline. On day 2, the mice were treated with Lico A and pirfenidone, respectively. On day 28, all of the mice were put to death. Then, lung tissues were collected and weighted. Pathological changes in lung tissue were measured by htoxylin eosin(HE) and Masson staining. The α-smooth muscle actin(α-SMA), Collagen I, fibronectin p-Smad2/3 and Smad2/3 were analyzed by Western blot. Then, transforming growth factor-β1 (TGF-β1)-induced MRC-5 cells were employed for evaluating the inhibitory activity of Lico A in vitro. Result: Compared with normal group, several pathological changes, including alveolar space collapse, emphysema, infiltration of inflammatory cells, and collagen deposition were observed in the BLM-treated mice, and these pathological changes were markedly attenuated by subsequent treatment with Lico A. Lico A could significantly inhibit BLM-induced up-regulation of α-SMA and Collagen I and phosphorylation of Smad2/3 in lung tissues of mice(PPβ-induced α-SMA and fibronectin expression in MRC-5 cells(PPConclusion: The preliminary mechanisms of the anti-fibrosis effect of Lico A may inhibit TGF-β/Smad pathway.