Effect of Cinnamomum Cassia on Cartilage Protection in Rabbit and Human Articular Cartilage

  • Baek, Yong-Hyeon (An Oriental Medicine Research Center for Bone & Joint Disease) ;
  • Huh, Jeong-Eun (Department of Acupuncture & Moxibustion, College of Oriental Medicine, Kyung Hee University) ;
  • Lee, Jae-Dong (An Oriental Medicine Research Center for Bone & Joint Disease) ;
  • Choi, Do-Young (An Oriental Medicine Research Center for Bone & Joint Disease) ;
  • Park, Dong-Suk (An Oriental Medicine Research Center for Bone & Joint Disease, Department of Acupuncture & Moxibustion, College of Oriental Medicine, Kyung Hee University)
  • Published : 2007.12.30

Abstract

Background & Objective: Articular cartilage is a potential target for drugs designed to inhibit the activity of matrix metalloproteinases (MMPs) to stop or slow the destruction of the proteoglycanand collagen in the cartilage extracellular matrix. The purpose of this study was to investigate the effects of Cinnamomum cassia in inhibiting the release of glycosaminoglycan (GAG), the degradation of collagen, and MMP activity in rabbit and human articular cartilage explants. Methods: The cartilage-protective effects of Cinnamomum cassia were evaluated by using glycosaminoglycan degradation assay, collagen degradation assay, colorimetric analysis of MMP activity, measurement of lactate dehydrogenase activity and histological analysis in rabbit cartilage explants culture. Results: Interleukin-1a (IL-1a) rapidly induced GAG, but collagen was much less readily released from cartilage explants. Cinnamomum cassia significantly inhibited GAG and collagen release in a concentration-dependent manner. Cinnamomum cassia dose-dependently inhibited MMP-1, MMP-3 and MMP-13 activities from IL-1a-treated cartilage explants culture when tested at concentrations ranging from 0.02 to 1 mg/ml. Conclusion : These results indicate that Cinnamomum cassia inhibits the degradation of proteoglycan and collagen through the down regulation of MMP-1, MMP-3 and MMP-13 activities of IL-1a-stimulated rabbit and human articular cartilage explants.

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