The protective effect of sophocarpine in osteoarthritis: An in vitro and in vivo study

被引:15
作者
Wu, Dengying [1 ,2 ]
Zhu, Xingyu [3 ]
Kang, Xiaodiao [1 ,2 ]
Huang, Huasong [3 ]
Yu, Jiale [3 ]
Pan, Jun [1 ,2 ]
Zhang, Xutong [4 ]
机构
[1] Wenzhou Med Univ, Affiliated Hosp 2, Dept Orthopaed Surg, 109 Xueyuanxi Rd, Wenzhou 325027, Peoples R China
[2] Wenzhou Med Univ, Yuying Childrens Hosp, 109 Xueyuanxi Rd, Wenzhou 325027, Peoples R China
[3] Wenzhou Med Univ, Clin Med Sch 2, 82 Xueyuanxi Rd, Wenzhou 325027, Peoples R China
[4] Wen Zhou Med Univ, Affiliated Hosp 2, Dept Anesthesiol, 109 Xueyuanxi Rd, Wenzhou 325027, Peoples R China
关键词
AKT; Inflammation; NF-kappa B; Osteoarthritis; PI3K; Sophocarpine; ARTICULAR-CARTILAGE; EXTRACELLULAR-MATRIX; SIGNALING PATHWAY; TNF-ALPHA; EXPRESSION; IL-1-BETA; MECHANISM; AGGRECAN; COX-2; MODEL;
D O I
10.1016/j.intimp.2018.11.046
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background: Osteoarthritis (OA) is a type of degenerative joint disease affecting millions of individuals world-wide. However, there are currently no great inflammatory treatments available for it. Sophocarpine (SPC), one of the key bioactive compounds derived from Sophora flavescens, has shown remarkable anti-inflammatory effects. Methods: In this study, we evaluated the effect of SPC on preventing the progression of OA and investigated its molecular target involved. In brief, rat chondrocytes were pretreated with SPC and subsequently stimulated with IL-1 beta. We found that SPC reduced the production of pro-inflammatory cytokines, such as nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-alpha), and interleukin-6 (IL-6). SPC also inhibited the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) at both the gene and protein level. Moreover, SPC promoted the expression of anabolic factors Sox-9 and aggrecan, while inhibiting the expression of catabolic factors, such as matrix metalloproteinases 13 (MMP-13) and thrombospondin motifs 5 (ADAMTS-5) in rat chondrocytes. Mechanistically, we found that SPC inhibited nuclear factor kappa B (NF-kappa B) via the phosphatidylinositol 3 kinase (PI3K)/AKT pathway. The beneficial effects of SPC were also observed in vivo using a rat OA model. Conclusions: Our findings indicate that SPC may be a potential novel therapeutic in the treatment of OA.
引用
收藏
页码:145 / 151
页数:7
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