Abstract
Idiopathic pulmonary fibrosis is a progressive and lethal form of interstitial lung disease that lacks effective therapies at present. Glycyrrhizic acid (GA), a natural compound extracted from a traditional Chinese herbal medicine Glycyrrhiza glabra, was recently reported to benefit lung injury and liver fibrosis in animal models, yet whether GA has a therapeutic effect on pulmonary fibrosis is unknown. In this study, we investigated the potential therapeutic effect of GA on pulmonary fibrosis in a rat model with bleomycin (BLM)-induced pulmonary fibrosis. The results indicated that GA treatment remarkably ameliorated BLM-induced pulmonary fibrosis and attenuated BLM-induced inflammation, oxidative stress, epithelial-mesenchymal transition, and activation of transforming growth factor-beta signaling pathway in the lungs. Further, we demonstrated that GA treatment inhibited proliferation of 3T6 fibroblast cells, induced cell cycle arrest and promoted apoptosis in vitro, implying that GA-mediated suppression of fibroproliferation may contribute to the anti-fibrotic effect against BLM-induced pulmonary fibrosis. In summary, our study suggests a therapeutic potential of GA in the treatment of pulmonary fibrosis.
Highlights
Idiopathic pulmonary fibrosis (IPF) is a progressive, usually fatal, form of interstitial lung disease of unknown etiology
The results demonstrated that Glycyrrhizic acid (GA) treatment significantly ameliorated BLM-induced pulmonary fibrosis, inflammation, oxidative stress, epithelialmesenchymal transition (EMT) and activation of transforming growth factor-beta (TGF-β) signaling pathway in the lungs
GA Attenuated BLM-induced Pulmonary Fibrosis in Rats Pulmonary fibrosis was primarily assessed by the histomorphological examination following hematoxylin and eosine (H&E) staining of the lung sections
Summary
Idiopathic pulmonary fibrosis (IPF) is a progressive, usually fatal, form of interstitial lung disease of unknown etiology. IPF is characterized by areas of peripheral fibrosis, interstitial inflammation, failure of alveolar re-epithelialization, persistence of fibroblasts/myofibroblasts, and deposition of extracellular matrix (ECM) molecules in the lung, and it resembles the histopathological pattern of usual interstitial pneumonitis (UIP; White et al, 2003). Clusters of fibroblasts with an activated myofibroblast phenotype are transiently present in the granulation tissue, namely fibroblast foci, and they represent microscopic zones where fibroblasts migrate, proliferate, and secrete ECM proteins that provide a tissue scaffold for the repair process (Lorena et al, 2002). Fibroblast foci have long been described in IPF (Katzenstein and Myers, 1998), and fibroblasts/myofibroblasts are recognized to be the key effector cells in fibrogenesis and in the pathogenesis of IPF (White et al, 2003)
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