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Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation.
Sci Rep. 2016 10 24; 6:35696.SR

Abstract

Aberrant activation of TGF-β1 is frequently encountered and promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. The present study investigated whether emodin mediates its effect via suppressing TGF-β1-induced EMT and fibroblast activation in bleomycin (BLM)-induced pulmonary fibrosis in rats. Here, we found that emodin induced apoptosis and inhibited cellular proliferation, migration and differentiation in TGF-β1-stimulated human embryonic lung fibroblasts (HELFs). Emodin suppressed TGF-β1-induced EMT in a dose- and time-dependent manner in alveolar epithelial A549 cells. Emodin also inhibited TGF-β1-induced Smad2, Smad3 and Erk1/2 activation, suggesting that Smad2/3 and Erk1/2 inactivation mediated the emodin-induced effects on TGF-β1-induced EMT. Additionally, we provided in vivo evidence suggesting that emodin apparently alleviated BLM-induced pulmonary fibrosis and improved pulmonary function by inhibiting TGF-β1 signaling and subsequently repressing EMT, fibroblast activation and extracellular matrix (ECM) deposition. Taken together, our data suggest that emodin mediates its effects mainly via inhibition of EMT and fibroblast activation and thus has a potential for the treatment of pulmonary fibrosis.

Authors+Show Affiliations

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.Department of Gastroenterology, Zhongshan Hospital, Fudan University, Shanghai, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China. Shanghai Key Laboratory of Medical Imaging Computing and Computer Assisted Intervention, Fudan University, Shanghai, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27774992

Citation

Guan, Ruijuan, et al. "Emodin Ameliorates Bleomycin-induced Pulmonary Fibrosis in Rats By Suppressing Epithelial-mesenchymal Transition and Fibroblast Activation." Scientific Reports, vol. 6, 2016, p. 35696.
Guan R, Wang X, Zhao X, et al. Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation. Sci Rep. 2016;6:35696.
Guan, R., Wang, X., Zhao, X., Song, N., Zhu, J., Wang, J., Wang, J., Xia, C., Chen, Y., Zhu, D., & Shen, L. (2016). Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation. Scientific Reports, 6, 35696. https://doi.org/10.1038/srep35696
Guan R, et al. Emodin Ameliorates Bleomycin-induced Pulmonary Fibrosis in Rats By Suppressing Epithelial-mesenchymal Transition and Fibroblast Activation. Sci Rep. 2016 10 24;6:35696. PubMed PMID: 27774992.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation. AU - Guan,Ruijuan, AU - Wang,Xia, AU - Zhao,Xiaomei, AU - Song,Nana, AU - Zhu,Jimin, AU - Wang,Jijiang, AU - Wang,Jin, AU - Xia,Chunmei, AU - Chen,Yonghua, AU - Zhu,Danian, AU - Shen,Linlin, Y1 - 2016/10/24/ PY - 2016/08/25/received PY - 2016/10/03/accepted PY - 2016/10/25/pubmed PY - 2018/4/19/medline PY - 2016/10/25/entrez SP - 35696 EP - 35696 JF - Scientific reports JO - Sci Rep VL - 6 N2 - Aberrant activation of TGF-β1 is frequently encountered and promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. The present study investigated whether emodin mediates its effect via suppressing TGF-β1-induced EMT and fibroblast activation in bleomycin (BLM)-induced pulmonary fibrosis in rats. Here, we found that emodin induced apoptosis and inhibited cellular proliferation, migration and differentiation in TGF-β1-stimulated human embryonic lung fibroblasts (HELFs). Emodin suppressed TGF-β1-induced EMT in a dose- and time-dependent manner in alveolar epithelial A549 cells. Emodin also inhibited TGF-β1-induced Smad2, Smad3 and Erk1/2 activation, suggesting that Smad2/3 and Erk1/2 inactivation mediated the emodin-induced effects on TGF-β1-induced EMT. Additionally, we provided in vivo evidence suggesting that emodin apparently alleviated BLM-induced pulmonary fibrosis and improved pulmonary function by inhibiting TGF-β1 signaling and subsequently repressing EMT, fibroblast activation and extracellular matrix (ECM) deposition. Taken together, our data suggest that emodin mediates its effects mainly via inhibition of EMT and fibroblast activation and thus has a potential for the treatment of pulmonary fibrosis. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/27774992/Emodin_ameliorates_bleomycin_induced_pulmonary_fibrosis_in_rats_by_suppressing_epithelial_mesenchymal_transition_and_fibroblast_activation_ L2 - https://doi.org/10.1038/srep35696 DB - PRIME DP - Unbound Medicine ER -