Hart P H, Brand C, Carson C F, Riley T V, Prager R H, Finlay-Jones J J
Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University, Adelaide, Australia.
Inflamm Res. 2000 Nov;49(11):619-26. doi: 10.1007/s000110050639.
To evaluate potential antiinflammatory properties of tea tree oil, the essential oil steam distilled from the Australian native plant, Melaleuca alternifolia.
The ability of tea tree oil to reduce the production in vitro of tumour necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, IL-8, IL-10 and prostaglandin E2 (PGE2) by lipopolysaccharide (LPS)-activated human peripheral blood monocytes was examined.
Tea tree oil emulsified by sonication in a glass tube into culture medium containing 10% fetal calf serum (FCS) was toxic for monocytes at a concentration of 0.016% v/v. However, the water soluble components of tea tree oil at concentrations equivalent to 0.125% significantly suppressed LPS-induced production of TNFalpha, IL-1beta and IL-10 (by approximately 50%) and PGE2 (by approximately 30%) after 40 h. Gas chromatography/mass spectrometry identified terpinen-4-ol (42 %), a-terpineol (3 %) and 1,8-cineole (2%, respectively, of tea tree oil) as the water soluble components of tea tree oil. When these components were examined individually, only terpinen-4-ol suppressed the production after 40 h of TNFalpha, IL-1beta, IL-8, IL-10 and PGE2 by LPS-activated monocytes.
The water-soluble components of tea tree oil can suppress pro-inflammatory mediator production by activated human monocytes.
评估茶树油的潜在抗炎特性,茶树油是从澳大利亚本土植物互叶白千层中水蒸气蒸馏得到的精油。
检测茶树油对脂多糖(LPS)激活的人外周血单核细胞体外产生肿瘤坏死因子-α(TNFα)、白细胞介素(IL)-1β、IL-8、IL-10和前列腺素E2(PGE2)的影响。
在含有10%胎牛血清(FCS)的培养基中,通过超声乳化于玻璃管中的茶树油,浓度为0.016%(v/v)时对单核细胞有毒性。然而,茶树油的水溶性成分在相当于0.125%的浓度下,40小时后能显著抑制LPS诱导的TNFα、IL-1β和IL-10(约50%)以及PGE2(约30%)的产生。气相色谱/质谱分析确定萜品-4-醇(42%)、α-萜品醇(3%)和1,8-桉叶素(分别占茶树油的2%)为茶树油的水溶性成分。单独检测这些成分时,只有萜品-4-醇能抑制LPS激活的单核细胞在40小时后产生TNFα、IL-1β、IL-8、IL-10和PGE2。
茶树油的水溶性成分可抑制活化的人单核细胞产生促炎介质。