Juglanin inhibits IL-1β-induced inflammation in human chondrocytes

被引:47
作者
Chen, Xinxin [1 ]
Zhang, Chengyong [2 ]
Wang, Xiao [1 ]
Huo, Shousong [1 ]
机构
[1] Henan Univ, Huaihe Hosp, Dept Orthopaed, 25 Minglun St, Kaifeng 475000, Henan, Peoples R China
[2] Second Peoples Hosp Nanyang City, Dept Orthopaed, Nanyang, Henan, Peoples R China
关键词
Osteoarthritis; juglanin; antiinflammation; chondrocytes; NF-kappa B; OSTEOARTHRITIS; CYTOKINES;
D O I
10.1080/21691401.2019.1657877
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Osteoarthritis (OA) is one of the most characterized joint diseases associated with chondrocyte apoptosis. Juglanin has been reported to have anti-inflammation activity. This study aimed to evaluate the protective anti-inflammatory effects of juglanin in human OA chondrocytes. Human OA chondrocytes were pretreated with juglanin (10, 20 and 40 mu m) for 2 h and subsequently stimulated with IL-1 beta for 24 h. Nitric oxide (NO) production was determined using the Griess method and prostaglandin E2 (PGE2), matrix metalloproteinase-3, -9 and -13 (MMP-3, MMP-9 and MMP-13), TNE-alpha, and IL-6 were assessed using ELISA. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), a disintegrin and metalloproteinase with thrombospondin motifs-4 and -5 (ADAMTS-4 and ADAMTS-5) were detected by qRT-PCR and western blot analysis. NF-kappa B signalling molecules were detected by western blot analysis. The results showed that juglanin dose-dependently suppressed PGE2, NO, MMP1, MMP3, MMP13, TNF-alpha and IL-6 production induced by IL-1 beta. The expression of COX-2, iNOS, ADAMTS-4 and ADAMTS-5 induced by IL-1 beta were also suppressed by juglanin pretreatment. Western blot analysis showed that juglanin suppressed IL-1 beta-induced NE-kappa B activation. Taken together, we found that juglanin inhibits IL-1 beta-induced inflammation through the regulation of NF-kappa B signalling. Juglanin might be used as a therapeutic agent for treating OA.
引用
收藏
页码:3614 / 3620
页数:7
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