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Am J Physiol Lung Cell Mol Physiol 284: L720-L726, 2003. First published December 27, 2002; doi:10.1152/ajplung.00396.2002
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Vol. 284, Issue 5, L720-L726, May 2003

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 Terawaki2,3, Satoshi Ishii2, Tetsuji Tomita1, Hiroshi Yamamoto1, Kohei Hashizume3, Yasuyoshi Ouchi1, and Takao Shimizu2,4

Departments of 1 Geriatric Medicine, 2 Biochemistry and Molecular Biology, and 3 Pediatric Surgery, Graduate School of Medicine, University of Tokyo, and 4 Core Research for Evolutional Science and Technology of Japan Science and Technology Corporation, Tokyo 113, Japan

Acute 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 with ATK significantly attenuated lung injury, polymorphonuclear neutrophil sequestration, and deterioration of gas exchange caused by lipopolysaccharide 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.

acute respiratory distress syndrome; lipopolysaccharide; sepsis; eicosanoid; leukotriene


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