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Meng Li [1; 2] and Ya Li [2; 3; 4] and JianSheng Li [2; 3; 5] and Peng Zhao [2] and Yunping Bai [2; 5] and SuXiang Feng [2] and Xuefang Liu [2] and Yang Wang [2; 3] and Qingqing Bian [2; 3] and Junzi Li [2; 3]

Academic Editor: Gorkem Kismali

1, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China, bucm.edu.cn

2, Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment & Chinese Medicine Development of Henan Province, Henan University of Chinese Medicine, Zhengzhou, Henan 450000, China, henantcm.org

3, Institute for Respiratory Diseases, The First Affiliated Hospital, Henan University of Chinese Medicine, Zhengzhou, Henan 450000, China, henantcm.org

4, Central Laboratory, The First Affiliated Hospital, Henan University of Chinese Medicine, Zhengzhou, Henan 450000, China, henantcm.org

5, Institute for Geriatrics, Henan University of Chinese Medicine, Zhengzhou, Henan 450000, China, henantcm.org

Received Jul 18, 2017; Revised Oct 4, 2017; Accepted Oct 30, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Idiopathic pulmonary fibrosis (IPF) is an insidious and progressive disorder characterized by the aberrant deposition of extracellular matrix, which leads to irreversible destruction of lung architecture and dysfunction of gas exchange [1]. Recent studies suggested an increasing prevalence and increasing incidence of IPF [2, 3]. It is a fatal disease with a median survival estimated at 2–5 years from diagnosis. Nevertheless, currently available treatments, represented by pirfenidone, proved to have side effects and brought weighty economy burden [4, 5]. Therefore, novel therapeutic agents are needed urgently for the effective treatment of IPF.

IPF is a severe result of an aberrant injury repair process in lung tissue. This pathophysiologic dysregulation involves a complex interaction between epithelial injury, oxidative stress, coagulation disturbances, and inflammation, ultimately leading to transformation of several cell types into myofibroblasts and extracellular matrix deposition [6]. When encountering the invaders, alveolar epithelium can secrete tumor necrosis factor- (TNF-) α, the mediator of inflammatory signal pathway [7], which can amplify the inflammation response by the activation of nuclear factor- (NF-) κB transcription factor. The inflammation response is responsible for the recruitments of leukocyte and lymphocyte and the aggravation...
 
 
 
 
 

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