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和厚朴酚是一种低分子量天然产物,可防止人骨性关节炎软骨细胞中的炎症反应和软骨基质降解。

Honokiol, a low molecular weight natural product, prevents inflammatory response and cartilage matrix degradation in human osteoarthritis chondrocytes.

机构信息

Institute of Toxicology, College of Medicine, National Taiwan University, No.1, Jen-Ai Road, Section 1, Taipei, 10051, Taiwan.

出版信息

J Orthop Res. 2014 Apr;32(4):573-80. doi: 10.1002/jor.22577. Epub 2013 Dec 27.

DOI:10.1002/jor.22577
PMID:24375705
Abstract

Proinflammatory cytokine interleukin-1β (IL-1β) stimulates several mediators of cartilage degradation and plays an important role in the pathogenesis of osteoarthritis (OA). Honokiol, a low molecular weight natural product isolated from the Magnolia officinalis, has been shown to possess anti-inflammatory effect. Here, we used an in vitro model of cartilage inflammation to investigate the therapeutic potential of honokiol in OA. Human OA chondrocytes were cultured and pretreated with honokiol (2.5-10 µM) with or without IL-1β (10 ng/ml). Nitric oxide (NO) production was quantified by Griess reagent. Prostaglandin (PG)E2 , metalloproteinase-13 (MMP-13), and interleukin-6 (IL-6) productions were quantified by enzyme-linked immunosorbent assay. The expressions of collagen II, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and nuclear factor κB (NF-κB)-related signaling molecules were determined by Western blotting. Our data showed that IL-1β markedly stimulated the expressions of iNOS and COX-2 and the productions of NO, PGE2 , and IL-6, which could be significantly reversed by honokiol. Honokiol could also suppress the IL-1β-triggered activation of IKK/IκBα/NF-κB signaling pathway. Moreover, honokiol significantly inhibited the IL-1β-induced MMP-13 production and collagen II reduction. Taken together, the present study suggests that honokiol may have a chondroprotective effect and may be a potential therapeutic choice in the treatment of OA patients.

摘要

炎症细胞因子白细胞介素-1β(IL-1β)刺激几种软骨降解介质,在骨关节炎(OA)发病机制中起重要作用。厚朴酚是从厚朴中分离得到的一种低分子量天然产物,具有抗炎作用。在这里,我们使用软骨炎症的体外模型来研究厚朴酚在 OA 中的治疗潜力。培养人 OA 软骨细胞,并在有或没有 IL-1β(10ng/ml)的情况下用厚朴酚(2.5-10µM)预处理。通过 Griess 试剂定量测定一氧化氮(NO)的产生。通过酶联免疫吸附试验定量测定前列腺素(PG)E2、金属蛋白酶-13(MMP-13)和白细胞介素-6(IL-6)的产生。通过 Western blot 测定胶原 II、环氧化酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)和核因子κB(NF-κB)相关信号分子的表达。我们的数据表明,IL-1β 可显著刺激 iNOS 和 COX-2 的表达以及 NO、PGE2 和 IL-6 的产生,这些反应可被厚朴酚明显逆转。厚朴酚还可以抑制 IL-1β 触发的 IKK/IκBα/NF-κB 信号通路的激活。此外,厚朴酚还可显著抑制 IL-1β 诱导的 MMP-13 产生和胶原 II 减少。综上所述,本研究表明厚朴酚可能具有软骨保护作用,可能是治疗 OA 患者的潜在治疗选择。

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