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Int. J. Mol. Sci. 2017, 18(8), 1771; doi:10.3390/ijms18081771

Ac2-26, an Annexin A1 Peptide, Attenuates Ischemia-Reperfusion-Induced Acute Lung Injury

1
The Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 114, Taiwan
2
Department of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
3
Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei 114, Taiwan
4
Department of Internal Medicine, Taoyuan Armed Forces General Hospital, Taoyuan 325, Taiwan
5
Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
*
Authors to whom correspondence should be addressed.
Received: 25 June 2017 / Revised: 28 July 2017 / Accepted: 14 August 2017 / Published: 15 August 2017
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Abstract

Annexin A1 (AnxA1) is an endogenous protein that modulates anti-inflammatory processes, and its therapeutic potential has been reported in a range of inflammatory diseases. The effect of AnxA1 on ischemia-reperfusion (IR)-induced lung injury has not been examined. In this study, isolated, perfused rat lungs were subjected to IR lung injury induced by ischemia for 40 min, followed by reperfusion for 60 min. The rat lungs were randomly treated with vehicle (phosphate-buffered saline), and Ac2-26 (an active N-terminal peptide of AnxA1) with or without an N-formyl peptide receptor (FPR) antagonist N-Boc-Phe-Leu-Phe-Leu-Phe (Boc2). An in vitro study of the effects of Ac2-26 on human alveolar epithelial cells subjected to hypoxia-reoxygenation was also investigated. Administration of Ac2-26 in IR lung injury produced a significant attenuation of lung edema, pro-inflammatory cytokine production recovered in bronchoalveolar lavage fluid, oxidative stress, apoptosis, neutrophil infiltration, and lung tissue injury. Ac2-26 also decreased AnxA1 protein expression, inhibited the activation of nuclear factor-κB and mitogen-activated protein kinase pathways in the injured lung tissue. Finally, treatment with Boc2 abolished the protective action of Ac2-26. The results indicated that Ac2-26 had a protective effect against acute lung injury induced by IR, which may be via the activation of the FPR. View Full-Text
Keywords: acute lung injury; ischemia-reperfusion; Ac2-26; annexin A1; nuclear factor-κB acute lung injury; ischemia-reperfusion; Ac2-26; annexin A1; nuclear factor-κB
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MDPI and ACS Style

Liao, W.-I.; Wu, S.-Y.; Wu, G.-C.; Pao, H.-P.; Tang, S.-E.; Huang, K.-L.; Chu, S.-J. Ac2-26, an Annexin A1 Peptide, Attenuates Ischemia-Reperfusion-Induced Acute Lung Injury. Int. J. Mol. Sci. 2017, 18, 1771.

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