- Volume 28 Issue 6
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Regulatory mechanism of Angelica Gigas extract powder on matrix metalloproteinases in vitro and in vivo model
참당귀 추출분말이 in vitro and in vivo model에서 MMPs 조절 기전
- Received : 2015.10.21
- Accepted : 2015.11.13
- Published : 2015.12.25
The precise mechanism underlying the therapeutic efficacy of an extraction powder of Angelica gigas (AGE) for the treatment of degenerative osteoarthritis was investigated in primary cultured rabbit chondrocytes and in a monosodium-iodoacetate (MIA)-induced osteoarthritis rat model. The treatment with AGE (50 μg/mL) effectively inhibited NF-B activation. The anti-inflammatory mechanism was clarified by gelatin zymography and western blotting measurements of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) activities. The AGE (50 μg/mL) treatment significantly reduced MMP-9 activity. The constituents of AGE— decursinol, decursin, and decursinol angelate—were determined by LC-MS/MS after a 24 hr treatment of rabbit chondrocytes. The contents of the major products, decursin and decursinol angelate, were 3.62±0.47 and 2.14 ±0.36 μg/mg protein, respectively in AGE-treated (50 μg/mL) rabbit chondrocytes. An in vivo animal study on rats fed a diet containing 25, 50, and 100 mg/kg AGE for 3 weeks revealed a significant inhibition of the MMPs in the MIA-induced rat articular cartilage. The genetic expression of arthritic factors in the articular cartilage was examined by RT-PCR of collagen Type I, collagen Type II, aggrecan, and MMP (MMP3, MMP-9, MMP13). Specifically, AGE up-regulated the expression of collagen Type I, collagen Type II, and aggrecan and inhibited MMP levels at all tested concentrations. Collectively, AGE showed a strong specific site of action on MMP regulation and protected against the degeneration of articular cartilage via cellular regulation of MMP expression both in vitro and in vivo.
Angelica gigas;osteoarthritis;MMPs;Decursin;Decursinol angelate;ectract
- D. D. Dean, J. Martel-Pelletier, J. P. Pelletier, D. S. Howell and J. F. Jr. Woessner, J. Clin. Invest., 84, 678-685 (1989). https://doi.org/10.1172/JCI114215
- J. F. Jr, Woessner and Z. Gunja-Smith, J. Rheumatol, 27(Suppl), 99-101 (1991).
- J. Martel-Pelletier, R. McCollum, N. Fujimoto, K. Obata, J. M. Cloutier and J. P. Pelletier, Lab Invest, 70, 807-15 (1994).
- V. B. Kraus, Med. Clinics North Am., 81, 85-112 (1997). https://doi.org/10.1016/S0025-7125(05)70506-X
- D. Felson, Epidemiol Rev., 10, 1-28 (1988). https://doi.org/10.1093/oxfordjournals.epirev.a036019
- Ammon HRT. Phytomedicine, 17, 862-867 (2010). https://doi.org/10.1016/j.phymed.2010.03.003
- K. S. Ahn, W. S. Sim, I. K. Lee, Y. B. Seu and I. H. Kim, Planta Med., 63(4), 360-361 (1996).
- K. S. Ahn, W. S. Sim and I. H. Kim, Planta Med., 62(1), 7-9 (1996). https://doi.org/10.1055/s-2006-957785
- KHIDI. Health functional food industry development assistance report. Korea Health Industry Development Institute, Chungbuk, Korea. p 8 (2011).
- K. Sengupta, J. N. Kolla, A. V. Krishnaraju, N. Yalamanchili, C. V. Rao, T. Golakoti, S. Raychaudhuri and S. P. Raychaudhuri, Boswellia serrata extract. Mol Cell Biochem, 354, 189-197 (2011). https://doi.org/10.1007/s11010-011-0818-1
- B. Park, S. Prasad, V. Yadav, B. Sung and B. B. Aggarwal, PLoS One, 6, e26943 (2011). https://doi.org/10.1371/journal.pone.0026943
- S. Roy, S. Khanna, A. V. Krishnaraju, G. V. Subbaraju, T. Yasmin, D. Bagchi and C. K Sen, Antioxid Redox Sign, 8, 653-660 (2006). https://doi.org/10.1089/ars.2006.8.653