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Anesth Analg 2007;104:369-377
© 2007 International Anesthesia Research Society
doi: 10.1213/01.ane.0000252414.00363.c4

CRITICAL CARE AND TRAUMA

Posttreatment with Aspirin-Triggered Lipoxin A4 Analog Attenuates Lipopolysaccharide-Induced Acute Lung Injury in Mice: The Role of Heme Oxygenase-1

Sheng-Wei Jin, MD, PhD*{ddagger}, Li Zhang, PhD{dagger}, Qin-Quan Lian, MD{ddagger}, Dong Liu, MD, PhD*, Ping Wu, PhD{dagger}, Shang-Long Yao, MD*, and Du-Yun Ye, PhD{dagger}

From the {ddagger}Department of Anesthesiology, Second Affiliated Hospital, Wenzhou Medical College, Wenzhou, China; *Departments of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; and {dagger}Departments of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Address correspondence to Sheng-Wei Jin, MD, PhD, Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhon University of Science and Technology, 1277 Jiefang Rd., Wuhan, Hubei Province, People’s Republic of China, 430022. Address e-mail to jinshengwei{at}sohu.com.

BACKGROUND: We hypothesized that posttreatment with 15-epi-16-parafluoro-phenoxy lipoxin A4 (ATL) could attenuate lipopolysaccharide (LPS)-induced acute lung injury in mice.

METHODS: All the animals were randomly assigned to one of six groups (n = 6 per group). In the sham-vehicle group, mice were treated with 0.9% saline 60 min after they were challenged with saline. The sham-ATL group was identical to the sham-vehicle group except that ATL (0.7 mg/kg, IV) was administered, and the sham-ZnPP group was identical to the sham-vehicle group except that Zinc protoporphyrin IX (ZnPP, 25 mg/kg IV) was administered. In the LPS-vehicle group, mice were treated with vehicle 60 min after they were challenged with LPS. The LPS-ATL group was identical to the LPS-vehicle group but received ATL. The ZnPP-ATL-LPS group was identical to the LPS-ATL group, but ZnPP was administered 30 min before ATL.

RESULTS: Inhalation of LPS increased inflammatory cell counts, tumor necrosis factor-{alpha}, and protein concentration in bronchoalveolar lavage fluid and also induced lung histological injury and edema. Posttreatment with ATL inhibited tumor necrosis factor-{alpha}, nitric oxide, and malondialdehyde production, with the outcome of decreased pulmonary edema, lipid peroxidation, and the infiltration of neutrophils in lung tissues. In addition, ATL promoted the formation of heme oxygenase-1 in the lung tissues. Heme oxygenase-1 activity was also increased in the lung tissues after ATL stimulation. The beneficial effects of ATL were abolished by ZnPP.

CONCLUSIONS: This study demonstrates that posttreatment with ATL significantly reduces LPS-induced acute lung injury in mice.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2007 by the International Anesthesia Research Society.