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Original Research Article | OPEN ACCESS

Allicin Protects against Lipopolysaccharide-Induced Acute Lung Injury by Up-Regulation of Claudin-4

Yue-liang Zheng, Wen-wei Cai, Guang-zhao Yan, Yuan-zhan Xu, Mei-qi Zhang

Department of Emergency, Zhejiang Provincial People's Hospital, Hangzhou 310014, China;

For correspondence:-  Mei-qi Zhang   Email: meiqizhang1208@153.com   Tel:+86057185893631

Received: 8 January 2014        Accepted: 31 May 2014        Published: 25 July 2014

Citation: Zheng Y, Cai W, Yan G, Xu Y, Zhang M. Allicin Protects against Lipopolysaccharide-Induced Acute Lung Injury by Up-Regulation of Claudin-4. Trop J Pharm Res 2014; 13(7):1063-1069 doi: 10.4314/tjpr.v13i7.8

© 2014 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of allicin, an active component of garlic, on lipopolysaccharide (LPS)-induced acute lung injury.
Methods: Wistar rats were subjected to LPS intravenous injection with or without allicin treatment to induce acute lung injury (ALI) model. Also, A549 cells were stimulated with LPS in the presence and absence of allicin. HE staining was used to detect pathological changes in lung tissues. Enzyme-linked immunosorbent assay (ELISA) was performed to measure cytokine content. Cell viability was measured by CCK-8 and EdU incorporation assay. Genes expression was determined by real time polymerase chain reaction (PCR) and Western blot. Flow cytometry was applied to measure cell apoptosis.
Results: In vivo data showed that pulmonary edema, inflammatory cytokines expression and pathological changes were significantly attenuated in LPS-induced ALI after treatment with allicin (p < 0.05) while in vitro results indicate that allicin administration significantly improved the A549 cell viability in a dose-dependent manner as measured by CCK-8 and EdU incorporation assay. Besides, flow cytometry analysis showed that cell apoptosis rate was significantly reduced in a concentration-dependent manner after allicin injection (30.3 vs. 11.8 %, p < 0.05). At the molecular level, allicin treatment dose-dependently up-regulated claudin-4 expression both in vivo and in vitro (p < 0.05).
Conclusion: The findings indicate that allicin can protect against LPS-induced ALI in vivo and in vitro probably by up-regulation of claudin-4 expression.

Keywords: Allicin, Acute lung injury, Lipopolysaccharide, Claudin-4, Up-regulation, Pulmonary edema, Inflammatory cytukines

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Thompson Reuters (ISI): 0.523 (2021)
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