Licochalcone A in Inhibiting Bleomycin-induced Pulmonary Fibrosis Through TGF-β/Smad Pathway
10.13422/j.cnki.syfjx.20190402
- VernacularTitle: 甘草查尔酮A通过调节TGF-β/Smad信号通路抑制小鼠肺纤维化
- Author:
Yu FU
1
;
Xia WU
2
;
Sui-qing CHEN
1
Author Information
1. School of Pharmacy, Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment & Chinese Medicine Development of Henan Province, Henan University of Chinese Medicine, Zhengzhou 450046, China
2. Henan Provincial People's Hospital, Zhengzhou 450000, China
- Publication Type:Research Article
- Keywords:
licochalcone A;
pulmonary fibrosis;
fibroblast;
transforming growth factor-β(TGF-β)/Smad
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2019;25(4):94-100
- CountryChina
- Language:Chinese
-
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(P<0.05, P<0.01). In addition, Lico A could significantly suppressed TGF-β-induced α-SMA and fibronectin expression in MRC-5 cells(P<0.05, P<0.01). Conclusion: The preliminary mechanisms of the anti-fibrosis effect of Lico A may inhibit TGF-β/Smad pathway.
