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桃叶珊瑚苷通过抑制RAW 264.7细胞中肿瘤坏死因子-α的产生发挥抗炎活性。

Anti-inflammatory activity of aucubin by inhibition of tumor necrosis factor-alpha production in RAW 264.7 cells.

作者信息

Park Kyoung Sik, Chang I-Moo

出版信息

Planta Med. 2004 Aug;70(8):778-9. doi: 10.1055/s-2004-827211.

DOI:10.1055/s-2004-827211
PMID:15326552
Abstract

To elucidate a possible mechanism for the anti-inflammatory action of iridoid glycosides, the effects of both aucubin (AU) and its hydrolyzed product (H-AU) by beta-glucosidase treatment were studied on the production of TNF-alpha in RAW 264.7 cells. H-AU suppressed the production of both mRNA for TNF-alpha and subsequent TNF-alpha protein in the culture, but AU did not. The production of TNF-alpha protein was inhibited in a dose-dependent manner with an IC (50) of 9.2 microM. In addition, treatment with H-AU blocked both the I-kappa B alpha degradation and the translocation of NF-kappa B from the cytosol fraction to the nuclear fraction (55 % inhibition) in the culture. However, treatment with H-AU did not affect the intracellular level of cAMP formed by forskolin treatment in human monocytes U937 culture, implying that there is no influence on the cAMP level in other cell systems. The present study indicates a possible justification for those medicinal plants containing iridoid glycoside that have been used for the treatment of inflammation.

摘要

为阐明环烯醚萜苷抗炎作用的可能机制,研究了桃叶珊瑚苷(AU)及其经β-葡萄糖苷酶处理后的水解产物(H-AU)对RAW 264.7细胞中肿瘤坏死因子-α(TNF-α)产生的影响。H-AU抑制了培养物中TNF-α mRNA及随后的TNF-α蛋白的产生,但AU没有。TNF-α蛋白的产生呈剂量依赖性抑制,半数抑制浓度(IC50)为9.2 μM。此外,用H-AU处理可阻断培养物中I-κBα的降解以及核因子-κB(NF-κB)从胞质组分向核组分的转位(抑制率55%)。然而,用H-AU处理对佛司可林处理的人单核细胞U937培养物中形成的细胞内环磷酸腺苷(cAMP)水平没有影响,这意味着对其他细胞系统中的cAMP水平没有影响。本研究为那些含有环烯醚萜苷且已用于治疗炎症的药用植物提供了可能的依据。

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