Biological and Pharmaceutical Bulletin
Online ISSN : 1347-5215
Print ISSN : 0918-6158
ISSN-L : 0918-6158
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Effect of Aralia cordata Extracts on Cartilage Protection and Apoptosis Inhibition
Yong-Hyeon BaekJeong-Eun HuhJae-Dong LeeDo-Young ChoiDong-Suk Park
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2006 年 29 巻 7 号 p. 1423-1430

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Cartilage loss in osteoarthritis is characterized by cartilage degradation and chondrocyte death. Cartilage degradation is induced by activation of matrix-metalloproteinases (MMPs) activity and degradation of glycosaminoglycan (GAG) and collagen. Also, chondrocyte death is induced by the apoptosis through the activation of MAP kinase and caspases activities. On the basis of this background, our study was designed to examine the cartilage protective and anti-apoptotic effect of Aralia cordata. Cartilage explants and Chondrocytes were cultured from rabbit knee joint cartilage and treated by 5 ng/ml IL-1α. Cartilage and chondroprotective effects of Aralia cordata were determined by measuring (1) GAG and collagen expression, (2) GAG and collagen degradation, (3) TIMP and MMPs expression, and (4) TIMP and MMPs activity. Anti-apoptotic effects of Aralia cordata were determined by measuring (1) JNK and p38 MAP kinase expression, (2) apoptotic cells by flow cytometry, and (3) caspase-3 activity. In cartilage explants and chondroctyes treated by IL-1α, Aralia cordata showed the decrease of GAG and collagen degradation, decrease of MMPs (MMP-1, -3, -13) activity, and increase of TIMP-1 activity in a dose-dependent manner. Aralia cordata also showed anti-apoptotic effect by inhibition of early and late apoptotic cells, sub-G1 phase cells, and caspase-3 activity through the downregulation of JNK and p38 MAP kinase signaling pathway. Aralia cordata inhibited the cartilage and chondrocyte destruction through the downregulation of MMPs activities and the inhibition of proteoglycan and collagen degradation. Also, Aralia cordata inhibited the chondrocyte apoptosis through the downregulation of JNK and p38 MAP kinase signal, and the inhibition of caspase-3 activity.

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© 2006 The Pharmaceutical Society of Japan
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