Tuberc Respir Dis.  2010 Feb;68(2):55-61. 10.4046/trd.2010.68.2.55.

Role of the PLA2-Activated Neutrophilic Oxidative Stress in Oleic Acid-Induced Acute Lung Injury

Affiliations
  • 1Department 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.

Keyword

Acute Lung Injury; Embolism, Fat; Neutrophils; Phospholipase A2

MeSH Terms

Acute Lung Injury
Animals
Embolism, Fat
Lung
Neutrophils
Oleic Acid
Oxidative Stress
Phospholipases A2
Quinacrine
Rats
Respiratory Burst
Oleic Acid
Phospholipases A2
Quinacrine
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