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J Surg Res. 2014 Jan;186(1):436-45. doi: 10.1016/j.jss.2013.09.003. Epub 2013 Sep 29.

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

Author information

1
Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, Jilin, PR China.

Abstract

BACKGROUND:

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.

MATERIALS AND METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

These findings suggested that bornyl acetate may be developed as a preventive agent for lung inflammatory diseases.

KEYWORDS:

Acute lung injury; Anti-inflammatory; Bornyl acetate; Lipopolysaccharide

PMID:
24120240
DOI:
10.1016/j.jss.2013.09.003
[Indexed for MEDLINE]

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