Role of Group II Phospholipase A2 in the Pulmonary Oxidative Stress of the Acute Lung Injury Induced by Gut Ischemia-Reperfusion.
- Author:
Sanghoon JHEON
1
;
Keun KIM
;
Sang Cheol LEE
;
Seong Eun KIM
;
Young Man LEE
;
Jong Tae LEE
Author Information
1. Department of Thoracic and Cardiovascular Surgery, School of Medicine, Catholic University of Daegu, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Respiratory distress syndrome;
Phospholipase A
- MeSH:
Acute Lung Injury*;
Bronchoalveolar Lavage;
Bronchoalveolar Lavage Fluid;
Constriction;
Edema;
Free Radicals;
Humans;
Hydrogen Peroxide;
Lung;
Mesenteric Artery, Superior;
Mesentery;
Microscopy;
Microscopy, Electron;
Neutrophils;
Oxidative Stress*;
Peroxidase;
Phospholipases A2*;
Phospholipases*;
Rats, Sprague-Dawley;
Reperfusion;
Respiratory Distress Syndrome, Adult;
Rutin
- From:The Korean Journal of Thoracic and Cardiovascular Surgery
2002;35(7):501-510
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The various pathogeneses of acute respiratory distress syndrome have been suggested but not established yet. In the present study, the role of group II phospholipase A2(PLA2) in the pathogenesis of gut ischemia-reperfusion(I/R) induced acute lung injury (ALI), especially in the pulmonary oxidative stress with infiltration of neutrophils was investigated. MATERIAL AND METHOD: To induce ALI, reperfusion of mesentery was done for 120 min after clamping of superior mesenteric artery for 60 min in Sprague-Dawley rats that weighed about 300g. To exmaine the role of group II PLA2 in ALI, especially endothelial injury associated with the action of neutrophils, lung myeloperoxidase activity, lung leak index, bronchoalveolar lavage fluid protein were measured, and pulmonary PLA2 activity changes in gut I/R were also measured. The role of group II PLA2 in the neutrophilic generation of free radicals was assessed by inhibiting group II PLA2 with rutin, manoalide and scalaradial. Furthermore, to verify the oxidative stress in the lung, histologic and free radical detecting cytochemical electron microscopy were done. RESULT: After reperfusion, ALI was developed with accumulation of neutrophils in the lung, which was confirmed by the increase of myeloperoxidase activity, lung leak index and bronchoalveolar lavage protein (p<0.001). The pulmonary and intestinal group II PLA2 activities significantly increased after gut I/R which were reversed by rutin(p<0.001). In vitro, cytochrome-c reduction assay denoted the inhibitory effects of rutin, scalaradial and manoalide on the production of free radicals from isolated human neutrophils. Histologically, neutrophilic accumulation and pericapillary edema in the lung after gut I/R was detected by light microscopy which was suppressed by rutin. In CeCl3 cytochemical electron microscopy, the increased production of hydrogen peroxide in the lung after gut I/R was confirmed and also the production of hydrogen peroxide was decreased by rutin. CONCLUSION: On the basis of these experimental results, the inhibition of group II PLA2 seemed to mitigate gut I/R-induced ALI by suppressing the production of free radicals from the infiltrated neutrophils. Collectively, group II PLA2 seems to play a crucial role in gut I/R-induced ALI by neutrophilic oxidative.
