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KMID : 0613820090190060818
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Journal of Life Science
2009 Volume.19 No. 6 p.818 ~ p.824
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Effect of Aspirin on the Acute Lung Injury Induced by Intestinal Ischemia/Reperfusion
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Park Yoon-Yub
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Abstract
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The mechanisms responsible for ischemia/reperfusion (I/R) injury have direct or indirect relevance to clinical lung injury after severe shock, cardiopulmonary bypass, and transplantation. This study investigated the effects of aspirin on intestinal I/R-induced acute lung injury (ALI) in rats. Lipopolysaccharide (LPS) induced cyclooxygenase-2 (COX-2) expression in A549 and RAW264.7 cells. RAW264.7 macrophages had shown greater expression of COX-2 than A549 cells. In addition, the NADPH oxidase inhibitor apocynin and p38 MAPK inhibitor SB203580 attenuated LPS-stimulated COX-2 expression. To induce ALI, intestinal ischemia was performed for 60 min prior to the 4 hr reperfusion by clamping the superior mesenteric artery in Sprague-Dawley rats. In order to test and compare the effect of non-specific COX inhibitor aspirin with the effect of mepacrine, a well known phospholipase A2 inhibitor, rats were divided into 4 groups: Sham, I/R, Mepa+I/R (mepacrine, 60 ㎎/㎏, i.p.), ASA+I/R (aspirin, 10 ㎎/㎏, i.p.). In the present investigation, myeloperoxidase activities in the lung and intestinal tissues were increased by I/R. These changes were reduced by single pretreatment of mepacrine (60 ㎎/㎏, i.p.) or aspirin (10 ㎎/㎏, i.p.) 30 min before I/R. Structural studies demonstrated that the tissue injuries in the lung and intestine after I/R were also attenuated by the pretreatment of mepacrine or aspirin. These results suggest that I/R-induced ALI is mediated, in part, by the activation of COX. In addition, pretreatment of aspirin might be helpful for the prevention of ALI in ARDS-prone patients. In addition, the p38 MAPK inhibitor and apocynin also might be helpful to ALI through the inhibition of COX-2 expression.
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KEYWORD
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Aspirin, cyclooxygenase-2, acute lung injury, ischemia-reperfusion injury
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