Anti-arthritic effects of chlorogenic acid in interleukin-1β-induced rabbit chondrocytes and a rabbit osteoarthritis model

作者：Chen, Wei-Ping; Tang, Jing-Li; Bao, Jia-Peng; Hu, Peng-Fei; Shi, Zhong-Li; Wu, Li-Dong^*

来源：International Immunopharmacology, 2011, 11(1): 23-28.

DOI：10.1016/j.intimp.2010.09.021

• Chlorogenic acid
• Osteoarthritis
• Matrix metalloproteinase
• Chondrocyte
• Interleukin-1 beta
• ACLT
• Nuclear factor kappa B

Cartilage degradation is one of the pathological changes of osteoarthritis (OA), and accumulating evidence suggests an excess of matrix metalloproteinases (MMPs) plays a role in this cartilage breakdown. Here, we investigated the effects of chlorogenic acid (CGA) on the mRNA and protein expression of MMPs in interleukin (IL)-1 beta-induced rabbit chondrocytes and evaluated the in vivo effects of CGA in experimental OA induced by anterior cruciate ligament transection (ACLT) in rabbits. Using quantitative real-time PCR and ELISA to investigate the expression levels of MMP-1, MMP-3, MMP-13, and tissue inhibitors of metalloproteinase-1 (TIMP-1) in IL-1 beta-induced rabbit chondrocytes, we showed that CGA inhibits the expression of these MMPs while increasing TIMP-1 expression, at both the mRNA and protein levels. In addition, IL-1 beta-induced activation of nuclear factor kappa B (NF-kappa B) and the degradation of inhibitor of kappa B (I kappa B)-alpha were suppressed by CGA. In rabbits, CGA decreased cartilage degradation as assessed by morphological and histological analyses. The down-regulation of MMP-1, MMP-3, and MMP-13 expression and up-regulation of TIMP-1 expression were also detected in CGA-treated cartilage compared with vehicle-treated cartilage, confirming these findings in an in vivo model. Taken together, these findings indicate that CGA may be considered as a possible candidate agent in the treatment of OA.

• 出版日期2011-1
• 单位浙江大学