期刊
TOXICOLOGY LETTERS
卷 262, 期 -, 页码 161-172出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2016.10.004
关键词
Emodin; Pulmonary fibrosis; Inflammation; Myofibroblast differentiation; Heat shock protein-47; Extracellular matrix deposition
类别
资金
- National Natural Science Foundation of China [81470203, 81500048]
Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease with few treatment options and poor prognosis. Emodin, extracted from Chinese rhubarb, was found to be able to alleviate bleomycin (BLM)-induced pulmonary fibrosis, yet the underlying mechanism remains largely unknown. This study aimed to further investigate the effects of emodin on the inflammation and fibrosis of BLM-induced pulmonary fibrosis and the mechanism involved in rats. Our results showed that emodin improved pulmonary function, reduced weight loss and prevented death in BLM-treated rats. Emodin significantly relieved lung edema and fibrotic changes, decreased collagen deposition, and suppressed the infiltration of myofibroblasts [characterized by expression of alpha-smooth muscle actin (alpha-SMA)] and inflammatory cells (mainly macrophages and lymphocytes). Moreover, emodin reduced levels of TNF-alpha, IL-6, TGF-beta 1 and heat shock protein (HSP)-47 in the lungs of BLM-treated rats. In vitro, emodin profoundly inhibited TGF-beta 1-induced alpha-SMA, collagen IV and fibronectin expression in human embryo lung fibroblasts (HELFs). Emodin also inhibited TGF-beta 1-induced Smad2/3 and STAT3 activation, indicating that Smad2/3 and STAT3 inactivation mediates emodin-induced effects on TGF-beta 1-induced myofibroblast differentiation. These results suggest that emodin can exert its anti-fibrotic effect via suppression of TGF-beta 1 signaling and subsequently inhibition of inflammation, HSP-47 expression, myofibroblast differentiation and extracellular matrix (ECM) deposition. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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