Abstract
To analyze the role of oxycodone in acute lung injury(ALI) induced by lipopolysaccharide (LPS) in rats. Male SD rats were randomly allocated into 4 groups: control group, oxycodone group, LPS group, LPS+ oxycodone group. The effects of oxycodone on LPS-induced neutrophils influx, inflammatory cytokines release, pulmonary edema, apoptotic cell were examined. In addition, the toll-like receptor 4 (TLR4) in lung tissues was detected by Western blotting. Oxycodone significantly attenuated LPS-induced pulmonary histopathologic changes, alveolar hemorrhage, and neutrophil infiltration. The lung wet-to-dry weight ratio, was markedly decreased by oxycodone(5.60±0.24 vs 6.80±0.27, P<0.05 ). Moreover, oxycodone decreased the productions of the inflammatory cytokines including IL-1β, TNF-α, HMGB-1((1 208±18)pg/ml, (1 660±14) pg/ml, (61±4) pg/ml , all P<0.05). Oxycodone treatment also reduced the concentration of apoptosis in lung tissues(18.6%±0.5%, P<0.05). Furthermore, the expression of TLR4 was significantly suppressed by oxycodone treatment in lung tissues(1.20±0.15, P<0.05). Oxycodone exerts protective effects on LPS-induced ALI in rats. The potential mechanism of this action may attribute partly to the inhibition of TLR4 activation.
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