RESUMO
Methyl phydroxycinnamate (MH), an esterified derivative of pCoumaric acid exerts antiinflammatory effects on lipopolysaccharide (LPS)stimulated RAW264.7 macrophages. Based on these effects, the present study investigated the protective role of MH in a mouse model of LPSinduced acute respiratory distress syndrome (ARDS). The results demonstrated that administration of LPS (5 mg/kg intranasally) markedly increased the neutrophil/macrophage numbers and levels of inflammatory molecules (TNFα, IL6, IL1ß and reactive oxygen species) in the bronchoalveolar lavage ï¬uid (BALF) of mice. On histological examination, the presence of inflammatory cells was observed in the lungs of mice administered LPS. LPS also notably upregulated the secretion of monocyte chemoattractant protein1 and protein content in BALF as well as expression of inducible nitric oxide synthase in the lungs of mice; it also caused activation of p38 mitogenactivated protein kinase (MAPK) and NFκB signaling. However, MH treatment significantly suppressed LPSinduced upregulation of inflammatory cell recruitment, inflammatory molecule levels and p38MAPK/NFκB activation, and also led to upregulation of heme oxygenase1 (HO1) expression in the lungs of mice. In addition, the ability of MH to induce HO1 expression was confirmed in RAW264.7 macrophages. Taken together, the findings of the present study indicated that MH may exert protective effects against airway inflammation in ARDS mice by inhibiting inflammatory cell recruitment and the production of inflammatory molecules.