Moxifloxacin Ameliorates Oleic Acid-induced Acute Lung Injury by Modulation of Neutrophilic Oxidative Stress in Rats.
10.4046/trd.2010.68.6.334
- Author:
Byung Yong KIM
1
;
Young Man LEE
Author Information
1. Department of Physiology, Daegu Catholic University School of Medicine, Daegu, Korea. leeym.cu.ac.kr
- Publication Type:Original Article
- Keywords:
Acute Lung Injury;
Neutrophils;
Oleic Acid;
Free Radicals;
Phospholipases A2, Secretory
- MeSH:
Acute Lung Injury;
Animals;
Aza Compounds;
Blotting, Western;
Bronchoalveolar Lavage Fluid;
Cerium;
Free Radicals;
Humans;
Immunohistochemistry;
Lung;
Male;
Neutrophils;
Oleic Acid;
Oxidative Stress;
Peroxidase;
Phagocytes;
Phospholipases A2, Secretory;
Pulmonary Edema;
Quinolines;
Rats;
Rats, Sprague-Dawley;
Respiratory Burst
- From:Tuberculosis and Respiratory Diseases
2010;68(6):334-344
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Based on the known immunoregulatory functions of moxifloxacin on phagocytes, the therapeutic effect of moxifloxacin on oleic acid (OA)-induced acute lung injury (ALI) was investigated. METHODS: Moxifloxacin (10 mg/kg) was given to male Sprague-Dawley rats that had been given oleic acid (OA, 30 microliter) intravenously. Five hours after OA injection, parameters demonstrating ALI were assessed to measure the effects of moxifloxacin on acute lung injury. RESULTS: The pathological findings of OA-induced ALI's was diminished by moxifloxacin. Through ultrastructural and CeCl3 EM histochemistry, moxifloxacin was confirmed to be effective in decreasing oxidative stress in the lung as well. Indices of ALI, such as lung weight/body weight ratio, protein content in bronchoalveolar lavage fluid, and lung myeloperoxidase were decreased by moxifloxacin. In diaminobenzidine immunohistochemistry, fluorescent immunohistochemistry, and Western blotting of the lung, moxifloxacin had decreased the enhanced expression of secretory phospholipase A2 (sPLA2) by OA. CONCLUSION: We concluded that moxifloxacin was effective in lessening acute inflammatory pulmonary edema caused by OA, by inhibiting the neutrophilic respiratory burst, which was initiated by the activation of sPLA2.
