Research: Sun Ten Ginseng Has a Protective Effect on Treatment of Cartilage Degradation of OA

 

Panax ginseng C.A. Meyer Modulates the Levels of MMP3

in S12 Murine Articular Cartilage Cell Line

 

Joon-Shik Shina, Namhee Parkb, Jehyeon Rac, Yangseok Kimb, Minkyu Shinb,

Moochang Hongb, Sung-Hoon Kimd, Ha-Jeong Kwonc, Seon-Pyo Hongc,

Jinju Kimc,, Hyunsu Baea,∗∗

 

a Jaseng Hospital of Oriental Medicine, Sinsa-dong, Kangnam-gu, Seoul 135-896, Republic of Korea

 

b Department of Physiology, College of Oriental Medicine, Kyung Hee University, #1 Hoeki-dong

 

Dongdaemoon-gu, Seoul 130-701, Republic of Korea

c Department of Oriental Pharmaceutical Sciences, Kyung Hee East-West Pharmaceutical Research Institute,

 

College of Pharmacy, Kyung Hee University, #1 Hoeki-dong Dongdaemoon-gu, Seoul 130-701, Republic of

Korea

d Department of Oriental Pathology, College of Oriental Medicine, Kyung Hee University, #1 Hoeki-dong

 

Dongdaemoon-gu, Seoul 130-701, Republic of Korea

 

Abstract


Aim of the study: The destruction of cartilage in patients with osteoarthritis occurs due to an imbalance between matrix synthesis and degradation. Cartilage degradation is induced by the activation of matrix metalloproteinases (MMPs). Therefore, this study was conducted to evaluate the cartilage protective effect of Panax ginseng C.A. Meyer (PG).

 

Materials and methods: S12 cells were treated with various concentrations of extract of PG and gensenosides Rd and Rb3 for 3 h, after which 10 ng/ml interleukin-1β (IL-1β) was added to the culturemedia. The levels of MMP3 in the conditioned media were then evaluated using an enzyme-linked immunosorbent assay (ELISA). In addition, reverse transcriptase-polymerase chain reaction (RT-PCR) was used to evaluate the mRNA expression of Type II Collagen and Pro-collagenase. Furthermore, Western blot analysis was performed to identify the roles that PG played in the ERK and p38 signaling pathways.

 

Results: The MMP3 secretion levels of S12 cells were significantly lowered in response to treatment with PG and gensenosides Rd and Rb3 at a concentration of 100μg/ml when compared to cells that were treated with IL-1β. In addition, PG induced the mRNA expression of Type II Collagen dose dependently. Furthermore, phosphorylated p38 and ERK were detected in S12 articular cartilage cell line that was treated with IL-1β. PG decreased the phosphorylation of p38, but PG did not exert any effect on phospho-ERK.

 

Conclusions: These findings indicate that PG and gensenosides Rd and Rb3 suppress MMP3 secretion and that gensenosides Rd and Rb3 are the major elements involved in the suppression of MMP3 by PG. Furthermore, the suppression of MMP3 by PG occurs via the inhibition of phospho-p38 activation. Therefore, PG may exert a protective effect against the cartilage degradation of OA.

 

© 2009 Elsevier Ireland Ltd. All rights reserved.


1.              Introduction

2.              Materials and methods

1.           Preparation of Korean Oriental Medicines: Jaseng-Ko is comprised of Rehmannia glutinosa Libschitz var. purpurea Makino, Achyranthes bidentata Blume, Panax ginseng C.A. Meyer, CERVI PANTOTRICHUM CORNU, Asini Gelatinum, and Poria cocos Wolf. The sprayed dried extracts of these 6 ingredients were purchased from the Sun Ten Pharmaceutical Company (Taipei, Taiwan).

2.           Reagents and antibodies

3.           Cell culture

4.           Treatment of S12 cells with IL-1β and Korean Oriental Medicines

5.           MTT assay

6.           Enzyme-linked immunosorbent assay (ELISA)

7.           RT-PCR analysis of gene expression

8.           Western blot analysis

9.           Statistical analysis

3.              Results

1.           Analysis of ginsenosides in PG

2.           Screening for MMP3 inhibition

3.           Cell viability in response to treatment with PG and Gensenosides

4.           Effects of PG on the induction of Type II Collagen mRNA in S12 cells

5.           Effects of PG on the reduction of p38 phosphorylation in S12 Cells

4.              Discussion

5.              Acknowledgements

6.              References

 

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