Inhibition of lung inflammatory responses by bornyl acetate is correlated with regulation of myeloperoxidase activity.

Bornyl acetate is a bicyclic monoterpene present in numerous conifer oils. In this study, we aimed at clarifying the potential anti-inflammatory function and mechanism of bornyl acetate by using lipopolysaccharide (LPS)-induced acute lung injury murine model and RAW 264.7 cells. RAW 264.7 cells were pretreated with bornyl acetate 1 h before LPS stimulation and cell-free super supernatants were collected to measure cytokine concentrations. To induce acute lung injury, BALB/c mice were injected intranasally with LPS and treated with bornyl acetate 1 h before LPS stimulation. Seven hours after administration, the bronchoalveolar lavage fluid (BALF) was collected for measuring the cell count and cytokine production. We collected lungs for assaying wet-to-dry weight ratio, myeloperoxidase activity, and histologic changes. The extent of phosphorylation of mitogen-activated protein kinases and nuclear factor κB was detected by Western blot. Our results showed that bornyl acetate downregulated the levels of proinflammatory cytokines in vitro and in vivo; reduced the number of total cells, neutrophils, and macrophages in BALF; attenuated the histologic alterations in the lung; decreased the wet-to-dry weight ratio in BALF; and suppressed NF-kappa-B inhibitor alpha, extracellular regulated protein kinases, c-JunN-terminal kinase, p38 mitogen-activated protein kinase activation. These findings suggested that bornyl acetate may be developed as a preventive agent for lung inflammatory diseases.