Polygonatum sibiricum polysaccharide inhibits IL-1β-induced inflammation in human chondrocytes

被引:9
|
作者
Wu, Jun [1 ]
Zhang, Xinyu [2 ]
Hu, Suqin [3 ]
Pan, Suohua [1 ]
Wang, Cunliang [4 ]
机构
[1] Eastern Theater Gen Hosp, Orthoped Dept, Nanjing, Peoples R China
[2] Peoples Liberat Army Gen Hosp, Med Ctr 4, Orthoped Dept, Beijing, Peoples R China
[3] Eastern Theater Gen Hosp, Outpatient Dept, Nanjing, Peoples R China
[4] Yangling Demonstrat Zone Hosp, Orthoped Dept, Xianyang, Peoples R China
来源
关键词
Osteoarthritis (OA); Polygonatum sibiricum polysaccharide (PSP); chondrocytes; inflammation; inflammatory; mediators; NF-KB signaling pathway; NF-KAPPA-B; OSTEOARTHRITIS; MEDIATORS; STATE;
D O I
10.1590/fst.44021
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Osteoarthritis (OA) is a degenerative joint disease associated with inflammation. Polygonatum sibiricum polysaccharide (PSP) is a major group of active components isolated from Polygonatum sibiricum with broad activities including anti-inflammatory effect. However, the role of PSP in OA is unclear. In the present study, we aimed to investigate the effects of PSP on IL-1 beta-induced inflammatory response in primary human OA chondrocytes. The results showed that PSP improved cell viability of chondrocytes in response to IL-1 beta induction. The increased levels of several inflammatory mediators including nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in IL-1 beta-induced chondrocytes were attenuated by PSP in a dose-dependent manner. The IL-1 beta-induced production of pro-inflammatory cytokines, TNF-alpha and IL-6, were mitigated by PSP in chondrocytes. Besides, PSP also suppressed the production of matrix metalloproteinases (MMPs), including MMP-1, MMP-3 and MMP-13 in IL-1 beta-stimulated chondrocytes. Furthermore, the IL-1 beta-induced activation of NF-KB signaling pathway in chondrocytes was also prevented by PSP. These findings suggested that PSP alleviated IL-1 beta-induced inflammatory response in chondrocytes via inhibiting NF-KB signaling pathway.
引用
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页数:7
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