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Int. J. Mol. Sci. 2014, 15(11), 19355-19368; doi:10.3390/ijms151119355

Emodin Ameliorates LPS-Induced Acute Lung Injury, Involving the Inactivation of NF-κB in Mice

1
Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, Department of Respiratory Medicine, West China Hospital of Sichuan University, Chengdu 610041, China
2
Respiratory Medicine, the First Affiliated Hospital of Chengdu Medical College, Chengdu 610500, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 15 August 2014 / Revised: 15 October 2014 / Accepted: 17 October 2014 / Published: 24 October 2014
(This article belongs to the Special Issue Signal Transduction of Tissue Repair)
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Abstract

Acute lung injury (ALI) and its severe manifestation of acute respiratory distress syndrome (ARDS) are well-known illnesses. Uncontrolled and self-amplified pulmonary inflammation lies at the center of the pathology of this disease. Emodin, the bio-active coxund of herb Radix rhizoma Rhei, shows potent anti-inflammatory properties through inactivation of nuclear factor-κB (NF-κB). The aim of this study was to evaluate the effect of emodin on lipopolysaccharide (LPS)-induced ALI in mice, and its potential bio-mechanism. In our study, BALB/c mice were stimulated with LPS to induce ALI. After 72 h of LPS stimulation, pulmonary pathological changes, lung injury scores, pulmonary edema, myeloperoxidase (MPO) activity, total cells, neutrophils, macrophages, TNF-α, IL-6 and IL-1β in bronchoalveolar lavage fluid (BALF), and MCP-1 and E-selectin expression were notably attenuated by emodin in mice. Meanwhile, our data also revealed that emodin significantly inhibited the LPS-enhanced the phosphorylation of NF-κB p65 and NF-κB p65 DNA binding activity in lung. Our data indicates that emodin potently inhibits LPS-induced pulmonary inflammation, pulmonary edema and MCP-1 and E-selectin expression, and that these effects were very likely mediated by inactivation of NF-κB in mice. These results suggest a therapeutic potential of emodin as an anti-inflammatory agent for ALI/ARDS treatment. View Full-Text
Keywords: emodin; acute lung injury (ALI); acute respiratory distress syndrome (ARDS); lipopolysaccharide (LPS); E-selectin; MCP-1; nuclear factor-κB (NF-κB) emodin; acute lung injury (ALI); acute respiratory distress syndrome (ARDS); lipopolysaccharide (LPS); E-selectin; MCP-1; nuclear factor-κB (NF-κB)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Xiao, M.; Zhu, T.; Zhang, W.; Wang, T.; Shen, Y.-C.; Wan, Q.-F.; Wen, F.-Q. Emodin Ameliorates LPS-Induced Acute Lung Injury, Involving the Inactivation of NF-κB in Mice. Int. J. Mol. Sci. 2014, 15, 19355-19368.

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