Scoparone prevents IL-1β-induced inflammatory response in human osteoarthritis chondrocytes through the PI3K/Akt/NF-κB pathway
Scoparone prevents IL-1β-induced inflammatory response in human osteoarthritis chondrocytes through the PI3K/Akt/NF-κB pathway
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DOI：
10.1016/j.biopha.2018.07.062
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发表时间：
2018-10-01
影响因子：
7.5
通讯作者：
Peng, Kan
中科院分区：
文献类型：
--
作者：
Lu, Chao;Li, Yanqi;Peng, Kan
骨关节炎（OA）是一种退行性关节疾病，通常伴有炎症。滨蒿内酯是从茵陈蒿中分离得到的具有抗炎活性的生物活性成分。然而，滨蒿内酯对OA炎症反应的影响尚未得到证实。本研究的目的是评估滨蒿内酯在体外OA中的作用。我们的研究结果表明，IL-1 β处理显着抑制软骨细胞的细胞活力，而抑制作用减弱滨蒿内酯以剂量依赖性的方式。IL-1 β还有效地诱导软骨细胞中一氧化氮（NO）、前列腺素E2（PGE 2）、MMP-3、MMP-13、ADAMTS-4和ADAMTS-5的产生。然而，滨蒿内酯剂量依赖性地抑制诱导。此外，滨蒿内酯抑制IL-1 β诱导的软骨细胞iNOS和考克斯-2的表达。此外，滨蒿内酯治疗可降低IL-1 β诱导的PI 3 K/Akt/NF-κ B通路的激活。综上所述，这些结果表明滨蒿内酯通过调节PI 3 K/Akt/NF-κ B通路抑制IL-1 β诱导的软骨细胞中炎症介质的表达。滨蒿内酯有望成为治疗骨关节炎的新药物。
Osteoarthritis (OA) is a degenerative joint disease that is commonly accompanied by inflammation. Scoparone is a biologically active constituent isolated from Artemisia capillaris and possesses anti-inflammatory activity. However, the effect of scoparone on inflammatory response in OA has not been authenticated. The aim of this study was to evaluate the role of scoparone in OA in vitro. Our results showed that IL-1 beta treatment significantly inhibited the cell viability of chondrocytes, whereas the inhibition effect was attenuated by scoparone in a dosedependent manner. IL-1 beta also efficiently induced the production of nitric oxide (NO), prostaglandin E2 (PGE2), MMP-3, MMP-13, ADAMTS-4 and ADAMTS-5 in chondrocytes. However, scoparone dose-dependently suppressed the induction. In addition, scoparone repressed IL-1 beta-induced the expression of iNOS and COX-2 in chondrocytes. Furthermore, the activation of the PI3K/Akt/NF-kappa B pathway induced by IL-1 beta was diminished by scoparone treatment. Taken together, these findings indicated that scoparone inhibited the expression of inflammatory mediators in IL-1 beta-induced chondrocytes via regulating the PI3K/Akt/NF-kappa B pathway. Thus, scoparone may be used as a new therapeutic agent for the treatment of OA.