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Kim J, Lee H, Kang KS, et al. Protective effect of Korean Red Ginseng against glucocorticoid-induced osteoporosis in vitro and in vivo. J Ginseng Res. 2014;39(1):46-53doi: 10.1016/j.jgr.2014.06.001.
Kim, J., Lee, H., Kang, K. S., Chun, K. H., & Hwang, G. S. (2015). Protective effect of Korean Red Ginseng against glucocorticoid-induced osteoporosis in vitro and in vivo. Journal of ginseng research, 39(1), 46-53. https://doi.org/10.1016/j.jgr.2014.06.001
Kim, Jinhee, et al. "Protective effect of Korean Red Ginseng against glucocorticoid-induced osteoporosis in vitro and in vivo." Journal of ginseng research vol. 39,1 (2015): 46-53. doi: https://doi.org/10.1016/j.jgr.2014.06.001
Kim J, Lee H, Kang KS, Chun KH, Hwang GS. Protective effect of Korean Red Ginseng against glucocorticoid-induced osteoporosis in vitro and in vivo. J Ginseng Res. 2015 Jan;39(1):46-53. doi: 10.1016/j.jgr.2014.06.001. Epub 2014 Jul 09. PMID: 25535476; PMCID: PMC4268568.
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J Ginseng Res. 2015 Jan;39(1):46-53. doi: 10.1016/j.jgr.2014.06.001. Epub 2014 Jul 09.

Protective effect of Korean Red Ginseng against glucocorticoid-induced osteoporosis in vitro and in vivo.

Journal of ginseng research

Jinhee Kim, Hyejin Lee, Ki Sung Kang, Kwang-Hoon Chun, Gwi Seo Hwang

Affiliations

  1. Laboratory of Cell Differentiation Research, College of Korean Medicine, Gachon University, Seongnam, Korea.
  2. College of Korean Medicine, Gachon University, Seongnam, Korea.
  3. Gachon Institute of Pharmaceutical Sciences, College of Pharmacy, Gachon University, Incheon, Korea.

PMID: 25535476 PMCID: PMC4268568 DOI: 10.1016/j.jgr.2014.06.001

Abstract

BACKGROUND: Glucocorticoids (GCs) are commonly used in many chemotherapeutic protocols and play an important role in the normal regulation of bone remodeling. However, the prolonged use of GCs results in osteoporosis, which is partially due to apoptosis of osteoblasts and osteocytes. In this study, effects of Korean Red Ginseng (KRG) on GC-treated murine osteoblastic MC3T3-E1 cells and a GC-induced osteoporosis mouse model were investigated.

METHODS: MC3T3-E1 cells were exposed to dexamethasone (Dex) with or without KRG and cell viability was measured by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Real-time polymerase chain reaction was performed to evaluate the apoptotic gene expression; osteogenic gene expression and alkaline phosphatase (ALP) activity were also measured. Western blotting was performed to evaluate the mitogen-activated protein kinase (MAPK) proteins. A GC-induced osteoporosis animal model was used for in vivo study.

RESULTS AND CONCLUSION: The MTT assay revealed that Korean Red Ginseng (KRG) prevents loss of cell viability caused by Dex-induced apoptosis in MC3T3E1 cells. Real-time polymerase chain reaction data showed that groups treated with both Dex and KRG exhibited lower mRNA levels of caspase-3 and -9, whereas the mRNA levels of Bcl2, IAPs, and XIAP increased. Moreover, groups treated with both Dex and KRG demonstrated increased mRNA levels of ALP, RUNX2, and bone morphogenic proteins as well as increased ALP activity in MC3T3-E1 cells, compared to cells treated with Dex only. In addition, KRG increased protein kinase B (AKT) phosphorylation and decreased c-Jun N-terminal kinase (JNK) phosphorylation. Moreover, microcomputed tomography analysis of the femurs showed that GC implantation caused trabecular bone loss. However, a significant reduction of bone loss was observed in the KRG-treated group. These results suggest that the molecular mechanism of KRG in the GC-induced apoptosis may lead to the development of therapeutic strategies to prevent and/or delay osteoporosis.

Keywords: Korean Red Ginseng; Panax ginseng; dexamethasone; osteoblast; osteoporosis

References

  1. Exp Cell Res. 2002 Apr 1;274(2):226-34 - PubMed
  2. Am J Med. 2000 Feb;108(2):153-64 - PubMed
  3. Biochim Biophys Acta. 2003 Sep 23;1642(1-2):79-85 - PubMed
  4. Crit Rev Eukaryot Gene Expr. 2003;13(2-4):221-35 - PubMed
  5. J Bone Miner Res. 2006 Apr;21(4):637-46 - PubMed
  6. Ann Clin Lab Sci. 2011 Fall;41(4):364-72 - PubMed
  7. J Ethnopharmacol. 2005 Oct 3;101(1-3):299-307 - PubMed
  8. Br J Pharmacol. 1995 Aug;115(7):1188-93 - PubMed
  9. Endocrinology. 2004 Apr;145(4):1835-41 - PubMed
  10. J Clin Invest. 1998 Jul 15;102(2):274-82 - PubMed
  11. Cancer Causes Control. 2000 Jul;11(6):565-76 - PubMed
  12. Nitric Oxide. 2005 May;12(3):159-62 - PubMed
  13. J Bone Miner Res. 2004 Mar;19(3):479-90 - PubMed
  14. Biol Pharm Bull. 1998 Aug;21(8):834-8 - PubMed
  15. Ann N Y Acad Sci. 2002 Jun;966:73-81 - PubMed
  16. Nutr Cancer. 2011 Nov;63(8):1339-47 - PubMed
  17. J Vet Med Sci. 2004 Feb;66(2):193-5 - PubMed
  18. Mol Cell Endocrinol. 2006 Mar 27;248(1-2):87-93 - PubMed
  19. J Ginseng Res. 2012 Apr;36(2):135-45 - PubMed
  20. Rev Endocr Metab Disord. 2001 Jan;2(1):65-73 - PubMed
  21. Food Chem Toxicol. 2011 Sep;49(9):2229-35 - PubMed
  22. J Ginseng Res. 2012 Jan;36(1):1-15 - PubMed
  23. Endocrinology. 1999 Nov;140(11):5339-47 - PubMed
  24. Rev Endocr Metab Disord. 2006 Jun;7(1-2):1-16 - PubMed
  25. Br J Pharmacol. 2006 Jul;148(6):860-70 - PubMed
  26. J Ginseng Res. 2013 Jul;37(3):261-8 - PubMed
  27. Arthritis Rheum. 2009 May;60(5):1427-37 - PubMed
  28. J Mol Cell Cardiol. 2012 Jan;52(1):237-44 - PubMed
  29. Bone. 1997 Jan;20(1):41-6 - PubMed
  30. Novartis Found Symp. 2001;232:23-36; discussion 36-46 - PubMed
  31. J Bone Joint Surg Am. 2002 Dec;84-A(12):2123-34 - PubMed
  32. Am J Orthop (Belle Mead NJ). 2003 Sep;32(9):429-36 - PubMed

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