Effects of Eugenol and Dehydrodieugenol B from <i>Nectandra leucantha</i> against Lipopolysaccharide (LPS)-Induced Experimental Acute Lung Inflammation.
Bittencourt-Mernak MI, Pinheiro NM, da Silva RC, Ponci V, Banzato R, Pinheiro AJMCR, Olivo CR, Tibério IFLC, Lima Neto LG, Santana FPR, Lago JHG, Prado CM.
Acute lung injury (ALI) is an important public health problem. The present work investigated whether dehydrodieugenol B treatment, a compound isolated from Brazilian plant <i>Nectandra leucantha</i> (Lauraceae), modulates experimental ALI and compared the observed effects to eugenol. Effects of dehydrodieugenol B <i>in vitro</i> in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells were evaluated. The lung and systemic inflammatory profile, lung function, and possible mechanisms involved in BALB/C male mice (6-8 weeks) with ALI induced by LPS instillation (5 mg/kg) was assayed. Dehydrodieugenol B did not affect the cell viability and inhibited the increase in NO release and IL-1β and IL-6 gene expression induced by LPS. <i>In vivo</i>, both compounds reduced lung edema, inflammatory cells, and the IL-6 and IL-1 β levels in bronchoalveolar lavage fluid, as well as reduced inflammatory cell infiltration and those positive to iNOS, MMP-9, and TIMP-1, and reduced the collagen content and the 8-isoprostane expression in lung tissue. Eugenol and dehydrodieugenol B also inhibited the phosphorylation of Jc-Jun-NH2 terminal Kinase (JNK), a signaling protein involved in the MAPKinase pathway. There was no effect of these compounds in lung function. Therefore, eugenol and dehydrodieugenol B ameliorates several features of experimental ALI and could be considered as a pharmacological tool to ameliorate acute lung inflammation.