Silibinin protects against osteoarthritis through inhibiting the inflammatory response and cartilage matrix degradation in vitro and in vivo
Autor: | Chunhui Chen, Liang Cheng, Yiting Lou, Hang Li, Zhenhua Feng, Wenhao Zheng, Xiaozhou Ying, Zhenyu Tao, Chuanxu Zhang |
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Jazyk: | angličtina |
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Silibinin Osteoarthritis Pharmacology Chondrocyte NF-κB Silybum marianum 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Protein kinase B Aggrecan silibinin biology business.industry Cartilage biology.organism_classification medicine.disease Nitric oxide synthase osteoarthritis 030104 developmental biology medicine.anatomical_structure Oncology chemistry inflammation 030220 oncology & carcinogenesis Immunology chondrocyte biology.protein business Research Paper |
Zdroj: | Oncotarget |
ISSN: | 1949-2553 |
Popis: | // Wenhao Zheng 1 , Zhenhua Feng 1 , Yiting Lou 1 , Chunhui Chen 1 , Chuanxu Zhang 1 , Zhenyu Tao 1 , Hang Li 1 , Liang Cheng 1 and Xiaozhou Ying 1 1 Department of Orthopaedic Surgery, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 325000, China Correspondence to: Xiaozhou Ying, email: yingxiaozhou@sina.com Keywords: osteoarthritis, chondrocyte, silibinin, inflammation, NF-κB Received: May 27, 2017 Accepted: August 04, 2017 Published: August 24, 2017 ABSTRACT Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage degradation and inflammation. Silibinin, a polyphenolic flavonoid derived from fruits and seeds of Silybum marianum , has been reported to possess various potent beneficial biological effects, such as antioxidant, anti-cancer, hepatoprotective and anti-inflammatory activities. However, the anti-inflammatory effects of silibinin on OA have not been reported. This study aimed to assess the effects of silibinin on OA both in vitro and in vivo . In this study, we found that silibinin significantly inhibited the nterleukin-1β (IL-1β)-induced production of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α) and IL-6, expression of cyclooxygenase2 (COX-2), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-1 (MMP-1), MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4) and ADAMTS-5, degradation of aggrecan and collagen-II in human OA chondrocytes. Furthermore, silibinin dramatically suppressed IL-1β-stimulated phosphatidylinositol 3 kinase/ protein kinase B (PI3K/Akt) phosphorylation and nuclear factor-kappa B (NF-kB) activation in human OA chondrocytes. In addition, treatment of silibinin not only prevented the destruction of cartilage and the thickening of subchondral bone but also relieved synovitis in mice OA models. Also, the immunohistochemistry results showed that silibinin significantly decreased the expression of MMP-13 and ADAMTS-5 and increased the expression of collagen-II and aggrecan in mice OA. Taken together, these results suggest that silibinin may be a potential agent in the treatment of OA. |
Databáze: | OpenAIRE |
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