Literature DB >> 27178341

Chitosan oligosaccharides inhibit IL-1β-induced chondrocyte apoptosis via the P38 MAPK signaling pathway.

Chun Zhang1, Ling Yu1, Yan Zhou1, Qi Zhao1, Shi-Qing Liu2.   

Abstract

The preventive and therapeutic effects of chitosan oligosaccharides (COS) on osteoarthritis (OA) have been rarely investigated. In this study, the protective effects of COS against IL-1β-induced chondrocyte apoptosis were evaluated and the underlying mechanisms were elucidated. Results showed that COS not only inhibited cell apoptosis in a dose-dependent manner but also ameliorated IL-1β-induced nuclear chromatin damage and mitochondrial membrane potential in chondrocytes. In IL-1β-treated chondrocytes, COS downregulated the expression of Bax and caspase-3 but upregulated the expression of Bcl-2 by inhibiting the phosphorylated p38 mitogen-activated protein kinase (MAPK). COS inhibited the mRNA expression of inducible nitric oxide synthase (iNOS) and matrix metalloproteinase-13 (MMP-13) and enhanced the mRNA expression of the tissue inhibitor of metalloproteinase-1 (TIMP-1). These results suggested that COS effectively inhibits the IL-1β-induced apoptosis of chondrocytes by activating the p38 MAPK signaling pathway. COS may also be used as a unique biological agent to prevent and treat OA.

Entities:  

Keywords:  Apoptosis; Chitosan oligosaccharide; Chondrocytes; Interleukin-1β; Matrix metalloproteinase; Osteoarthritis

Mesh:

Substances:

Year:  2016        PMID: 27178341     DOI: 10.1007/s10719-016-9667-1

Source DB:  PubMed          Journal:  Glycoconj J        ISSN: 0282-0080            Impact factor:   2.916


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