Abstract
To investigate the effects of propofol pretreatment on lung morphology and heme oxygenase-1 expression in oleic acid -induced acute lung injury in rats. A total of 32 male Sprague-Dawley rats (250-300g) were randomly divided into the following four groups (n=8/group): group C, group OA, group OA+PR, and group OA+IX to compare related parameter changes. PaO2, PCO2, and PaO2/FiO2 were significantly different among the four treatment groups (P<0.05 or P<0.01). Lung wet/dry weight ratio and HO-1 protein expression also significantly differed among the groups (P<0.01). Immunohistochemistry showed that the expression of HO-1 in group OA+PR was stronger than those in groups OA, OA+IX, and C. Light microscopy revealed that pathological changes in lung tissues in group OA+PR were milder than those in group OA and group OA+IX. Electron microscopy showed that alveolar type II epithelial cell ultrastructure in group OA was relatively irregular with cell degeneration and disintegration and cytoplasmic lamellar bodies were vacuolized. Changes in group OA+PR were milder than those in group OA; however, they were more severe in group OA+IX than in group OA. Propofol significantly increases the expression of HO-1 in the lung tissueand prevents changes in lung morphology due to ALI in rats.
Highlights
Acute lung injury (ALI) is a critical condition characterized by severe hypoxemia and respiratory distress
This study investigated the impact of propofol on the histomorphology of the lung in oleic acid (OA)induced ALI in rats and explored its possible mechanisms of action, aiming to provide evidence for clinical treatment
We evaluated the impact of propofol on OA-induced ALI in rats
Summary
Acute lung injury (ALI) is a critical condition characterized by severe hypoxemia and respiratory distress. Propofol is a fat-soluble intravenous anesthetic that exerts good antioxidant effects; its lung-protective roles have been verified[7,8,9]. It can regulate innate immunity and the expression of proinflammatory signals in sepsis[10,11]. It can reduce the expression of toll-like receptor 2/4 in sepsis[12,13], attenuate the expression of NF-κB in sepsis[14], and upregulate the expression ofHO-115. This study investigated the impact of propofol on the histomorphology of the lung in oleic acid (OA)induced ALI in rats and explored its possible mechanisms of action, aiming to provide evidence for clinical treatment
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