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紫云英苷通过抑制核因子κB(NF-κB)和丝裂原活化蛋白激酶(MAPK)的激活,抑制白细胞介素-1β(IL-1β)诱导的人骨关节炎软骨细胞中炎症介质的产生。

Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation.

作者信息

Ma Zhiqiang, Piao Taikui, Wang Yanlong, Liu Jianyu

机构信息

Department of Orthopedic Surgery, the Second Hospital of Harbin Medical University, Harbin, Heilongjiang Province 150086, People's Republic of China.

Children's Hospital of Harbin, Harbin, Heilongjiang Province 150010, People's Republic of China.

出版信息

Int Immunopharmacol. 2015 Mar;25(1):83-7. doi: 10.1016/j.intimp.2015.01.018. Epub 2015 Jan 28.

DOI:10.1016/j.intimp.2015.01.018
PMID:25637445
Abstract

Astragalin, a bioactive component isolated from Rosa agrestis, has been described to exhibit anti-inflammatory activity. The aim of this study was to investigate the anti-inflammatory effects and the underlying mechanisms of astragalin on IL-1β-stimulated human osteoarthritis chondrocyte. The production of NO and PGE2 was detected by Griess reaction and ELISA. The expression of iNOS and COX-2 was detected by western blotting. The expression of NF-κB and MAPKs was detected by western blot analysis. We found that astragalin dose-dependently inhibited IL-1β-induced NO and PGE2 production, as well as iNOS and COX-2 expression. Meanwhile, western blot analysis showed that astragalin inhibited IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte. In addition, astragalin was found to activate PPAR-γ. The inhibition of astragalin on IL-1β-induced NO and PGE2 production can be reversed by PPAR-γ antagonist GW9662. Astragalin suppressed IL-1β-induced inflammatory mediators via activating PPAR-γ, which subsequently inhibited IL-1β-induced NF-κB and MAPK activation. Astragalin may be a potential agent in the treatment of osteoarthritis.

摘要

黄芪苷是从野蔷薇中分离出的一种生物活性成分,已被描述具有抗炎活性。本研究的目的是探讨黄芪苷对白细胞介素-1β刺激的人骨关节炎软骨细胞的抗炎作用及其潜在机制。通过格里斯反应和酶联免疫吸附测定法检测一氧化氮(NO)和前列腺素E2(PGE2)的产生。通过蛋白质免疫印迹法检测诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的表达。通过蛋白质免疫印迹分析检测核因子κB(NF-κB)和丝裂原活化蛋白激酶(MAPKs)的表达。我们发现黄芪苷剂量依赖性地抑制白细胞介素-1β诱导的NO和PGE2的产生,以及iNOS和COX-2的表达。同时,蛋白质免疫印迹分析表明黄芪苷抑制白细胞介素-1β诱导的人骨关节炎软骨细胞中NF-κB和MAPK的激活。此外,发现黄芪苷可激活过氧化物酶体增殖物激活受体γ(PPAR-γ)。PPAR-γ拮抗剂GW9662可逆转黄芪苷对白细胞介素-1β诱导的NO和PGE2产生的抑制作用。黄芪苷通过激活PPAR-γ抑制白细胞介素-1β诱导的炎症介质,随后抑制白细胞介素-1β诱导的NF-κB和MAPK激活。黄芪苷可能是治疗骨关节炎的一种潜在药物。

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