Protective mechanisms of sevoflurane against one-lung ventilation-induced acute lung injury: role of cyclooxygenase-2 and 5-lipoxygenase pathways.
- Author:
Rui LIU
1
;
Jing LUO
;
Jiang LI
;
Qingjie MA
;
Jingzhe SUN
;
Yanhua LI
;
Dianhua WANG
Author Information
- Publication Type:Journal Article
- MeSH: Acute Lung Injury; etiology; metabolism; Animals; Arachidonate 5-Lipoxygenase; metabolism; Cyclooxygenase 2; metabolism; Lung; drug effects; metabolism; Methyl Ethers; adverse effects; One-Lung Ventilation; adverse effects; RNA, Messenger; genetics; Rabbits
- From: Journal of Southern Medical University 2013;33(5):625-630
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo explore the protective mechanisms of sevoflurane against acute lung injury (ALI) induced by one-lung ventilation (OLV) in view of cyclooxygenase-2 (COX2) and 5-lipoxygenase (5-LOX) pathways.
METHODEighteen healthy Japanese white rabbits were randomized into sham-operated group (S group), OLV group (O group) and OLV + sevoflurane group (OS group). COX2 and 5-LOX protein and mRNA expressions in the lungs were detected by Western blotting and real-time PCR, respectively. Prostaglandin I2 (PGI2), thromboxane A2 (TXA2) and leukotrienes B2 (LTB2) in the lung tissues were quantified with ELISA. Histological scores and lung wet/dry weight (W/D) ratios were determined for lung injury assessment.
RESULTSCOX2 and 5-LOX protein and mRNA expressions and the contents of LTB2, TXA2 and PGI2 in the lungs, lung W/D ratio and histological scores were significantly higher while PGI2/TXA2 ratio was significantly lower in O group and OS group than in S group (P<0.05). Compared with those in O group, COX2 and 5-LOX expressions, pulmonary contents of LTB2, TXA2 and PGI2, and lung W/D ratio all decreased significantly but PGI2/TXA2 ratio was significantly elevated in OS group (P<0.05).
CONCLUSIONOLV may activate COX2 and 5-LOX pathways to result in increased production of arachidonic acid metabolites. Sevoflurane protects against OLV-induced ALI probably by reducing AA metabolites and regulating PGI2/TXA2 ratio through inhibitions of COX2 and 5-LOX pathways.