Tuberc Respir Dis > Volume 68(2); 2010 > Article
Tuberculosis and Respiratory Diseases 2010;68(2):55-61.
DOI: https://doi.org/10.4046/trd.2010.68.2.55    Published online February 1, 2010.
Role of the PLA2-Activated Neutrophilic Oxidative Stress in Oleic Acid-Induced Acute Lung Injury.
Young Man Lee, Byung Yong Kim, Yoon Yub Park
Department of Physiology, Catholic University of Daegu School of Medicine, Daegu, Korea. leeym@cu.ac.kr
Abstract
BACKGROUND
The underlying pathogenesis of fat embolism-induced acute lung injury (ALI) has not been elucidated. In the present study, the pathogenesis of fat embolism-induced ALI was probed in association with neutrophilic oxidative stress in oleic acid (OA)-induced ALI of S-D rats. METHODS: OA was injected intravenously to provoke ALI in experimental rats. Five hours later, indices of ALI were measured to confirm the role of the neutrophilic respiratory burst. The effect of an inhibition of phospholipase A2 (PLA2) was also evaluated. RESULTS: The accumulation of neutrophils in the lung due to OA caused increased neutrophilic oxidative stress in lung, which was ameliorated by mepacrine. What were the results from inhibition of PLA2. CONCLUSION: Excess neutrophilic oxidative stress contributes to OA-induced ALI, which is lessened by the inhibition of PLA2.
Key Words: Acute Lung Injury, Embolism, Fat, Neutrophils, Phospholipase A2


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