The water-soluble components of the essential oil of Melaleuca alternifolia (tea tree oil) suppress the production of superoxide by human monocytes, but not neutrophils, activated in vitro

被引:104
作者
Brand, C
Ferrante, A
Prager, RH
Riley, TV
Carson, CF
Finlay-Jones, JJ
Hart, PH
机构
[1] Flinders Univ S Australia, Sch Med, Dept Microbiol & Infect Dis, Adelaide, SA 5001, Australia
[2] Womens & Childrens Hosp, Dept Immunopathol, Adelaide, SA 5006, Australia
[3] Flinders Univ S Australia, Sch CHem Phys & Earth Sci, Adelaide, SA 5001, Australia
[4] Univ Western Australia, Dept Microbiol, Nedlands, WA 6907, Australia
关键词
tea tree oil; monocytes; neutrophils; oxygen derived reactive species; superoxide production;
D O I
10.1007/s000110050746
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Objective: To evaluate the regulatory properties of the essential oil of Melaleuca alternifolia (tea tree oil) on the production of oxygen derived reactive species by human peripheral blood leukocytes activated in vitro. Materials and methods: The ability of tea tree oil to reduce superoxide production by neutrophils and monocytes stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP), lipopolysaccharide (LPS) or phorbol 12-myristate 13-acetate (PMA) was examined. Results: The water-soluble fraction of tea tree oil had no significant effect on agonist-stimulated superoxide production by neutrophils, but significantly and dose-dependently suppressed agonist-stimulated superoxide production by monocytes. This suppression was not due to cell death. Chemical analysis identified the water-soluble components to be terpinen-4-ol, alpha -terpineol and 1,8-cineole. When examined individually, terpinen-4-ol significantly suppressed fMLP- and LPS- but not PMA-stimulated superoxide production; cr-terpineol significantly suppressed fMLP-, LPS- and PMA-stimulated superoxide production; 1,8-cineole was without effect. Conclusion: Tea tree oil components suppress the production of superoxide by monocytes, but not neutrophils, suggesting the potential for selective regulation of cell types by these components during inflammation.
引用
收藏
页码:213 / 219
页数:7
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