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Med Sci Monit. 2018 Jan 1;24:1-10.

Emodin Attenuates Bleomycin-Induced Pulmonary Fibrosis via Anti-Inflammatory and Anti-Oxidative Activities in Rats.

Author information

1
The Hospital of Wuhan University of Science and Technology, Wuhan, Hubei, China (mainland).
2
Tianyou Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, Hubei, China (mainland).
3
Medical School, Wuhan University of Science and Technology, Wuhan, Hubei, China (mainland).
4
Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China (mainland).

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.

PMID:
29290631
PMCID:
PMC5759514
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