LAUSR

Emodin is a natural anthraquinone compound, which is the main component found in the traditional Chinese herb Polygonum cuspidatum. The anti‐fibrosis effects of Emodin have been reported. This study aimed to explore the specific mechanism of Emodin in the epithelial‐mesenchymal transition (EMT) of pulmonary fibrosis. The pulmonary fibrosis mice models were constructed with bleomycin, the EMT models of alveolar epithelial cells were stimulated by TGF‐β1, and Emodin was used for intervention. c‐MYC and miR‐182‐5p were overexpressed or silenced by cell transfection. Our results demonstrated that Emodin attenuated pulmonary fibrosis induced by bleomycin in mice, and inhibited EMT, meanwhile downregulated c‐MYC, upregulated miR‐182‐5p, and downregulated ZEB2 in vitro and vivo. Next, overexpression of c‐MYC promoted EMT, while silencing c‐MYC and overexpressing miR‐182‐5p inhibited EMT. Then, c‐MYC negatively regulated the expression of miR‐182‐5p with a direct binding relationship. And miR‐182‐5p inhibited ZEB2 expression in a targeted manner. Finally, Emodin inhibited EMT that had been promoted by overexpression of c‐MYC. In conclusion, Emodin could attenuate pulmonary fibrosis and EMT by regulating the c‐MYC/miR‐182‐5p/ZEB2 axis, which might provide evidence for the application of Emodin in the treatment of pulmonary fibrosis.