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. 2012 Dec 15:12:256.
doi: 10.1186/1472-6882-12-256.

Standardized butanol fraction of WIN-34B suppresses cartilage destruction via inhibited production of matrix metalloproteinase and inflammatory mediator in osteoarthritis human cartilage explants culture and chondrocytes

Jeong-Eun Huh  1 , Byung-Kwan Seo, Yong-Hyeon Baek, Sanghoon Lee, Jae-Dong Lee, Do-Young Choi, Dong-Suk Park
Affiliations

Standardized butanol fraction of WIN-34B suppresses cartilage destruction via inhibited production of matrix metalloproteinase and inflammatory mediator in osteoarthritis human cartilage explants culture and chondrocytes

Jeong-Eun Huh et al. BMC Complement Altern Med. .

Abstract

Background: WIN-34B is a novel Oriental medicine, which represents the n-butanol fraction prepared from dried flowers of Lonicera japonica Thunb and dried roots of Anemarrhena asphodeloides BUNGE. The component herb of WIN-34B is used for arthritis treatment in East Asian countries. The aim of this study was to determine the cartilage-protective effects and mechanisms of WIN-34B and its major phenolic compounds, chlorogenic acid and mangiferin, in osteoarthritis (OA) human cartilage explants culture and chondrocytes.

Methods: The investigation focused on whether WIN-34B and its standard compounds protected cartilage in interleukin (IL)-1β-stimulated cartilage explants culture and chondrocytes derived from OA patients. Also, the mechanisms of WIN-34B on matrix metalloproteinases (MMPs), tissue inhibitor of matrix metalloproteinases (TIMPs), inflammatory mediators, and mitogen-activated protein kinases (MAPKs) pathways were assessed.

Results: WIN-34B was not cytotoxic to cultured cartilage explants or chondrocytes. WIN-34B dose-dependently inhibited the release of glycosaminoglycan and type II collagen, increased the mRNA expression of aggrecan and type II collagen, and recovered the intensity of proteoglycan and collagen by histological analysis in IL-1β-stimulated human cartilage explants culture. The cartilage protective effect of WIN-34B was similar to or better than that of chlorogenic acid and mangiferin. Compared to chlorogenic acid and mangiferin, WIN-34B displayed equal or greater decreases in the levels of MMP-1, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5, and markedly up-regulated TIMP-1 and TIMP-3. WIN-34B inhibited inflammatory mediators involved in cartilage destruction, such as prostaglandin E2, nitric oxide, tumor necrosis factor-alpha, and IL-1β. The phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and p38 was significantly reduced by WIN-34B treatment, while phosphorylation of JNK was only inhibited by chlorogenic acid or mangiferin in IL-1β-stimulated chondrocytes.

Conclusions: WIN-34B is potentially valuable as a treatment for OA by virtue of its suppression of MMPs, ADAMTSs, and inflammatory mediators, and it's up-regulation of TIMP-1 and TIMP-3 involved in the MAPK pathway.

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Figures

Figure 1
Figure 1
Representative HPLC chromatogram of the extracts of WIN-34B and its standard compounds. HPLC chromatogram of WIN-34B (A), major compound of chlorogenic acid (B) and mangiferin (C). Chlorogenic acid was detected at approximately 14 min and mangiferin was detected at approximately 18 min at 254 nm in this system.
Figure 2
Figure 2
Effect of WIN-34B and its major compounds on the cytotoxicity of IL-1β-stimulated human cartilage explants culture and chondrocytes.
Figure 3
Figure 3
Effect of WIN-34B and its major compounds on cartilage protection of IL-1β-stimulated human cartilage explants culture.
Figure 4
Figure 4
Histochemical analysis of proteoglycan and collagen in IL-1β-stimulated human cartilage explants culture.
Figure 5
Figure 5
Effect of WIN-34B and its major compounds on the level of matrix proteinases and tissue inhibitor of matrix proteinases in human cartilage explants.
Figure 6
Figure 6
Effect of WIN-34B and its major compounds on the productions of inflammatory mediators in IL-1β-stimulated cartilage explants culture.
Figure 7
Figure 7
Effect of WIN-34B and its major compounds on pERK, pJNK, and pp38 MAPK proteins in IL-1β-stimulated human cartilage explants.
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References

    1. Krasnokutsky S, Attur M, Palmer G, Samuels J, Abramson SB. Current concepts in the pathogenesis of osteoarthritis. Osteoarthr Cartil. 2008;16(Suppl 3):S1–S3. - PubMed
    1. Tetlow LC, Adlam DJ, Woolley DE. Matrix metalloproteinase and proinflammatory cytokine production by chondrocytes of human osteoarthritic cartilage: associations with degenerative changes. Arthritis Rheum. 2001;44(3):585–594. doi: 10.1002/1529-0131(200103)44:3<585::AID-ANR107>3.0.CO;2-C. - DOI - PubMed
    1. Fernandes JC, Martel-Pelletier J, Pelletier JP. The role of cytokines in osteoarthritis pathophysiology. Biorheology. 2002;39(1–2):237–246. - PubMed
    1. Goldring MB, Goldring SR. Osteoarthritis. J Cell Physiol. 2007;213(3):626–634. doi: 10.1002/jcp.21258. - DOI - PubMed
    1. Goldring MB, Otero M. Inflammation in osteoarthritis. Curr Opin Rheumatol. 2011;23(5):471–478. doi: 10.1097/BOR.0b013e328349c2b1. - DOI - PMC - PubMed

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