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β-桉叶醇的调节机制是通过抑制肥大细胞介导的炎症反应中的半胱天冬酶-1 的激活。

The regulatory mechanism of β-eudesmol is through the suppression of caspase-1 activation in mast cell-mediated inflammatory response.

机构信息

Department of Medicinal Herb Development, Gyeongju University, Gyeongbuk, Republic of Korea.

出版信息

Immunopharmacol Immunotoxicol. 2011 Mar;33(1):178-85. doi: 10.3109/08923973.2010.491082. Epub 2010 Jul 6.

Abstract

β-Eudesmol is sesquiterpenoid alcohol which contains the rhizome of Atractylodes lancea. Although it has multiple pharmacological effects, the anti-inflammatory effect of β-eudesmol and its molecular mechanisms are poorly elucidated. In this study, we investigated the regulatory mechanism of β-eudesmol on mast cell-mediated inflammatory response. The results indicated that β-eudesmol inhibited the production and expression of interleukin (IL)-6 on phorbol 12-myristate 13-acetate and calcium ionophore A23187-stimulated human mast cell (HMC). In activated HMC-1 cells, β-eudesmol suppressed activation of p38 mitogen-activated protein kinase (MAPKs) and nuclear factor-κB. In addition, β-eudesmol suppressed the activation of caspase-1 and expression of receptor-interacting protein-2. These results provide new insights into the pharmacological actions of β-eudesmol as a potential molecule for use in therapy in mast cell-mediated inflammatory diseases.

摘要

β-桉叶醇是倍半萜醇,存在于苍术根茎中。尽管它具有多种药理作用,但β-桉叶醇的抗炎作用及其分子机制尚不清楚。在这项研究中,我们研究了β-桉叶醇对肥大细胞介导的炎症反应的调节机制。结果表明,β-桉叶醇抑制佛波醇 12-肉豆蔻酸 13-乙酸酯和钙离子载体 A23187 刺激的人肥大细胞(HMC)中白细胞介素(IL)-6 的产生和表达。在激活的 HMC-1 细胞中,β-桉叶醇抑制丝裂原活化蛋白激酶(MAPK)和核因子-κB 的激活。此外,β-桉叶醇抑制半胱天冬酶-1的激活和受体相互作用蛋白-2 的表达。这些结果为β-桉叶醇作为肥大细胞介导的炎症性疾病治疗的潜在分子的药理作用提供了新的见解。

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