Abstract

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) can severely damage lung function, which may result in death. Emodin is a major ingredient of rhubarb and has been proven to protect against lung disruptions. Our study focused on the potential medicinal effect of emodin against IPF.

MATERIAL AND METHODS: The experiment subjects were fully-grown male Sprague-Dawley rats with average weight of 180–220 kg. Histological analyses, Western blotting analysis, quantitative real-time PCR, and statistical analysis were used in the study.

RESULTS: We found that emodin significantly reduced lung structural distortion, collagen overproduction, massive inflammatory cells infiltration, proinflammatory cytokines expansion, and injuries caused by administration of bleomycin (BLM). Additionally, emodin suppressed the accumulation of p-IκBα and NF-κB, while stimulating the Nrf2-antioxidant signaling process in damaged lungs. Emodin inhibited epithelial-mesenchymal transition (EMT) induced by BLM in the lungs. Moreover, emodin suppressed the TGF-β1 expression and the downstream signal molecules p-Smad-2 and p-Smad-3, which are reinforced by BLM. Emodin can also reverse EMT-like shifts induced by recombinant TGF-β1 in alveolar epithelial cultured cells.

CONCLUSIONS: The effect of emodin in fibrotic lung injury is closely related to its favorable properties of anti-inflammation and anti-oxidation.

Keywords: Emodin, Epithelial-mesenchymal transition, idiopathic pulmonary fibrosis