Effect of oxycodone on acute lung injury induced by lipopolysaccharide in rats

Abstract

Objective To evaluate the effect of oxycodone on acute lung injury (ALI) induced by lipopolysaecharide (LPS) in rats. Methods Thirty-six pathogen-free healthy male Sprague-Dawley rats, weighing 250-300 g, were divided into 3 groups (n=12 each) using a random number table: sham operation group (group S), LPS-induced ALI group (group A) and oxycodone group (group O). ALI was induced by injecting LPS 8 mg/kg intravenously in A and O groups, while the equal volume of normal saline was given instead in group S. Oxycodone 2 mg/kg was injected intravenously at 10 min before LPS injection in group O, while the equal volume of normal saline was given instead in S and A groups.Rats were sacrificed at 6 h after LPS injection, and the broncho-alveolar lavage fluid (BALF) was collected for detection of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) concentrations by enzyme-linked immunosorbent assay.Pulmonary specimens were obtained for microscopic examination of the pathological changes and for determination of wet/dry weight ratio (W/D ratio) and expression of Toll-like receptor 4 (TLR4) in lung tissues (using real-time polymerase chain reaction and Western blot). Results Compared with group S, the TNF-α and IL-1β concentrations in BALF, W/D ratio, pathological scores and expression of TLR4 were significantly increased at 6 h after LPS injection in A and O groups (P<0.05). Compared with group A, the TNF-α and IL-1β concentrations in BALF, W/D ratio, pathological scores and expression of TLR4 were significantly decreased at 6 h after LPS injection in group O (P<0.05). Conclusion Oxycodone can attenuate LPS-induced ALI in lung tissues, and the mechanism is related to down-regulating the expression of TLR4 and inhibiting inflammatory responses of rats. Key words: Oxycodone; Endotoxemia; Respiratory distress syndrome, adult