Protective Effect of Sinomenine on Cartilage Degradation and Chondrocytes Apoptosis
-
- JU Xiao-dong
- Institute of Sports Medicine, Peking University Third Hospital
-
- DENG Min
- Department of Neurology, Peking University Third Hospital
-
- AO Ying-fang
- Institute of Sports Medicine, Peking University Third Hospital
-
- YU Chang-long
- Institute of Sports Medicine, Peking University Third Hospital
-
- WANG Jian-quan
- Institute of Sports Medicine, Peking University Third Hospital
-
- YU Jia-kuo
- Institute of Sports Medicine, Peking University Third Hospital
-
- CUI Guo-qing
- Institute of Sports Medicine, Peking University Third Hospital
-
- HU Yue-lin
- Institute of Sports Medicine, Peking University Third Hospital
Search this article
Abstract
Sinomenine (SIN), an alkaloid extracted from the stem of the Chinese medicinal plant sinomenium acutum, has been used for treating rheumatoid arthritis. But little is known whether SIN has a protective effect on osteoarthritis (OA). In this study, we investigated the protective effect of SIN on IL-1β-induced proteoglycan degradation and apoptosis in rabbit articular cartilage and chondrocytes. Treatment with 10 ng/ml IL-1β increased the level of glycosaminoglycan (GAG) released into the culture media, and up-regulated the activity and mRNA expression of matrix metalloproteinase 13 (MMP-13) and down-regulated the activity and mRNA expression of tissue inhibitor of metalloproteinase 1 (TIMP-1) in cartilage explants, as confirmed by the methods of GAG quantitation, MMP-13/TIMP-1 enzyme-linked immunosorbent assay (ELISA) and real-time quantitative RT-PCR. Treatment with 10 ng/ml IL-1β resulted in marked apoptosis in chondrocytes, as demonstrated by decreased cell viability, occurrence of DNA laddering and increased caspase-3 activity and annexin V binding of phosphatidylserine. However, simultaneous treatment with SIN (10, 50 or 250 μM) inhibited the GAG release and the activity and mRNA expression of MMP-13, and enhanced the activity and mRNA expression of TIMP-1 in a dose-dependent manner in cartilage explants. Furthermore, DNA fragment, caspase-3 activity and apoptosis rate were down-regulated, and cell viability was up-regulated dose-dependently in chondrocytes. Thus, SIN has the protective capacity to antagonize cartilage degradation and chondrocyte apoptosis, which suggest that SIN may act as an agent for pharmacological intervention in the progress of OA.<br>
Journal
-
- YAKUGAKU ZASSHI
-
YAKUGAKU ZASSHI 130 (8), 1053-1060, 2010-08-01
The Pharmaceutical Society of Japan
- Tweet
Keywords
Details 詳細情報について
-
- CRID
- 1390282681104942720
-
- NII Article ID
- 130000308771
-
- NII Book ID
- AN00284903
-
- ISSN
- 13475231
- 00316903
-
- NDL BIB ID
- 10794777
-
- Text Lang
- en
-
- Data Source
-
- JaLC
- NDL
- Crossref
- CiNii Articles
-
- Abstract License Flag
- Disallowed