Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressing lethal disease with few clinically effective therapies. Corilagin is a tannin derivative which shows anti-inflammatory and antifibrotics properties and is potentiated in treating IPF. Here, we investigated the effect of corilagin on lung injury following bleomycin exposure in an animal model of pulmonary fibrosis. Corilagin abrogated bleomycin-induced lung fibrosis as assessed by H&E; Masson’s trichrome staining and lung hydroxyproline content in lung tissue. Corilagin reduced the number of apoptotic lung cells and prevented lung epithelial cells from membrane breakdown, effluence of lamellar bodies and thickening of the respiratory membrane. Bleomycin exposure induced expression of MDA, IKKα, phosphorylated IKKα (p-IKKα), NF-κB P65, TNF-α and IL-1β, and reduced I-κB expression in mice lung tissue or in BALF. These changes were reversed by high-dose corilagin (100 mg/kg i.p) more dramatically than by low dose (10 mg/kg i.p). Last, corilagin inhibits TGF-β1 production and α-SMA expression in lung tissue samples. Taken together, these findings confirmed that corilagin attenuates bleomycin-induced epithelial injury and fibrosis via inactivation of oxidative stress, proinflammatory cytokine release and NF-κB and TGF-β1 signaling. Corilagin may serve as a promising therapeutic agent for pulmonary fibrosis.
Highlights
Idiopathic pulmonary fibrosis (IPF), featured by chronic exacerbating dyspnea and respiratory failure, affects 2–29 cases per 100,000 individuals [1,2]
The pathology of pulmonary fibrosis and IPF is characterized by exuberant apoptosis of lung epithelial cells and consequential fibrotic remodeling, which leads to irreversible distortion of the lung architecture and eventually honeycombing [5,6]
Breakdown of cell membrane and subcellular structures, effluence of lamellar bodies and thickening of respiratory membrane in ATII cells 24 h after bleomycin inhalation (Figures 5 and 6). These results were in line with previous studies, which showed the efficacy of reactive oxygen species (ROS) scavengers such as superoxide dismutase (SOD) and N-acetylcysteine in prevention of bleomycin-induced lung epithelial damage and fibrosis [15,16]
Summary
Idiopathic pulmonary fibrosis (IPF), featured by chronic exacerbating dyspnea and respiratory failure, affects 2–29 cases per 100,000 individuals [1,2]. Attenuation of free radicals and NF-κB signaling may be part of the mechanism of alleviating liver fibrosis by corilagin, but whether corilagin inhibits TGF-β1/Smad signaling and epithelial-mesenchymal transition has not been ascertained [27]. Based on these data, we hypothesized that corilagin might prevent lung epithelial cells from bleomycin-induced damage via eradiation of free radicals and inhibition of NF-κB signaling. The present study was to compare the impacts of corilagin in different dosage on epithelial injury in a mice model of aerosol bleomycin-induced pulmonary fibrosis. The findings would shed light on the effects of corilagin on bleomycin-induced lung epithelial damage and fibrosis, and unlock the possible mechanisms
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
