AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol (December 27, 2002). doi:10.1152/ajplung.00396.2002
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
284/5/L720    most recent
00396.2002v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nagase, T.
Right arrow Articles by Shimizu, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nagase, T.
Right arrow Articles by Shimizu, T.
Submitted on November 18, 2002
Accepted on December 25, 2002

A potent inhibitor of cytosolic phospholipase A2, arachidonyl trifluoromethyl ketone, attenuates LPS-induced lung injury in mice

Takahide Nagase1*, Naonori Uozumi2, Tomoko Aoki-Nagase1, Kan Terawaki3, Satoshi Ishii2, Tetsuji Tomita1, Hiroshi Yamamoto1, Kohei Hashizume4, Yasuyoshi Ouchi1, and Takao Shimizu5

1 Department of Geriatric Medicine, University of Tokyo, Graduate School of Medicine, Tokyo, Japan
2 Department of Biochemistry and Molecular Biology, University of Tokyo, Graduate School of Medicine, Tokyo, Japan
3 Department of Biochemistry and Molecular Biology, University of Tokyo, Graduate School of Medicine, Tokyo, Japan; Department of Pediatric Surgery, University of Tokyo, Graduate School of Medicine, Tokyo, Japan
4 Department of Pediatric Surgery, University of Tokyo, Graduate School of Medicine, Tokyo, Japan
5 Department of Biochemistry and Molecular Biology, University of Tokyo, Graduate School of Medicine, Tokyo, Japan; CREST of Japan Science and Technology Corporation, Japan

* To whom correspondence should be addressed. E-mail: takahide-tky{at}umin.ac.jp.

Adult respiratory distress syndrome (ARDS) is an acute lung injury of high mortality rate and sepsis syndrome is one of the most frequent causes of ARDS. Metabolites of arachidonic acid including thromboxanes and leukotrienes are proinflammatory mediators and potentially involved in the development of ARDS. A key enzyme for the production of these inflammatory mediators is cytosolic phospholipase A2 (cPLA2). Recently, it has been reported that arachidonyl trifluoromethyl ketone (ATK) is a potent inhibitor of cPLA2. In the present study, we hypothesized that pharmacological intervention of cPLA2 could affect acute lung injury. To test this hypothesis, we examined the effects of ATK in a murine model of acute lung injury induced by septic syndrome. The treatment of ATK significantly attenuated lung injury, PMN sequestration and deterioration of gas exchange caused by lipopolysaccharide (LPS) and zymosan administration. The current observations suggest that pharmacological intervention of cPLA2 could be a novel therapeutic approach to acute lung injury caused by sepsis syndrome.




This article has been cited by other articles:


Home page
 Infect. Immun.Home page
B. P. Hurley and B. A. McCormick
Multiple Roles of Phospholipase A2 during Lung Infection and Inflammation
Infect. Immun., June 1, 2008; 76(6): 2259 - 2272.
[Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
T. Miyahara, K. Hamanaka, D. S. Weber, M. Anghelescu, J. R. Frost, J. A. King, and J. C. Parker
Cytosolic phospholipase A2 and arachidonic acid metabolites modulate ventilator-induced permeability increases in isolated mouse lungs
J Appl Physiol, February 1, 2008; 104(2): 354 - 362.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2002 by the American Physiological Society.