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Effect of Phylloquinone on Dexamethasone-Induced Calcification of Heart Muscle and Media Elastocalcinosis in Aorta Artery in Rat Model

Received: 12 August 2015     Accepted: 8 September 2015     Published: 9 September 2015
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Abstract

Background. Dexamethasone is a type of steroid medication which enhances the rate of pericyte differentiation and mineralization in vitro with concomitant suppression of calcification inhibitory molecule matrix Gla-protein (MGP). Vitamin K is an essential cofactor in the carboxylation of glutamate residues in a small group of proteins, including MGP. This study tries to assess the efficacy of vitamin K1 on dexamethasone-induced media elastocalcinosis in aorta artery and heart muscle in a rat model. Materials and Methods. 110 male rats with a normal weight range of 270 ± 20 were enrolled in this study. They received a calcification-inducing diet containing both vitamin K1 and dexamethasone during 6 or 12 weeks and were randomly assigned into two groups; a basic group (n=30), and an experimental group (n=80). The experimental group was divided into two groups receiving treatment during 6 and 12 weeks. Administration of dexamethasone was 0.5 mg/kg, intraperitoneal (IP). Vitamin K intakes were different including 5, 10, and 20 µg/kg, which were considered as low, moderate, and high intake, respectively. Results. Plasma concentrations of calcium were not affected by the different regimes and ranged between 2.27 and 2.31 millimolar (mM) (mean ± SD: 2.29 ± 0.02). According to the findings of pathologic biopsy of aorta artery and heart muscle, treatment of 0.5 mg/kg dexamethasone during 6 and 12 weeks did not induce media elastocalcinosis at all. Conclusion. Administration of 0.5 mg/kg dexamethasone during 6 and 12 weeks did not induce media elastocalcinosis at all. On the other hand, structure and histology of vessels did not change following intake of vitamin K1, therefore, different dosages of vitamin K could not affect the aorta artery status.

Published in International Journal of Clinical and Experimental Medical Sciences (Volume 1, Issue 3)
DOI 10.11648/j.ijcems.20150103.15
Page(s) 60-64
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2015. Published by Science Publishing Group

Keywords

Media Elastocalcinosis, Dexamethasone, Vitamin K, Aorta Artery, Heart Muscle

References
[1] Schurgers LJ, Spronk HM, Soute BA, Schiffers PM, DeMey JG, Vermeer C. Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats. Blood. 2007;109:2823-2831.
[2] Vermer C, Braam L. Role of K vitamins in the regulation of tissue calcification. J Bone Miner Metab. 2001;19:201-206.
[3] Wallin R, Schurgers L, Wajih N. Effects of the blood coagulation vitamin K as an inhibitor of arterial calcification. Thrombosis Research. 2008;122:411-417.
[4] Spronk HM, Soute BA, Schurgers LJ, Thijssen HH, De Mey JG, Vermeer C. Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats. J Vasc Res. 2003;40:531–537.
[5] Thane CW, Paul AA, Bates CJ, Bolton-Smith C, Prentice A, Shearer MJ. Intake and sources of phylloquinone (vitamin K1): variation with socio-demographic and lifestyle factors in a national sample of British elderly people. Br J Nutr. 2002;87:605-613.
[6] McKeown NM, Jacques PF, Gundberg CM, et al. Dietary and nondietary determinants of vitamin K biochemical measures in men and women. J Nutr. 2002;132:1329-1334.
[7] Shanahan CM, Weissberg PL, Metcalfe JC. Isolation of gene markers of differentiated and proliferating vascular smooth muscle cells. Circ Res. 1993;73:193–204.
[8] Davidson RT, Foley AL, Engelke JA, Suttie JW. Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria. J Nutr. 1998;128:220-223.
[9] Willenberg T, Diehm N, Zwahlen M, et al. Impact of long-term corticosteroid therapy on the distribution pattern of lower limb atherosclerosis. Eur J Vasc Endovasc Surg. 2010;39:441-446.
[10] Nashel DJ. Is atherosclerosis a complication of long-term corticosteroid treatment? Am J Med. 1986;80:925-929.
[11] Miyahara T, Nemoto M, Tukamoto S, et al. Induction of metallothionein and stimulation of calcification by dexamethasone in cultured clonal osteogenic cells, MC3T3-E1. Toxicol Lett. 1991;57:257-267.
[12] Kirton JP, Wilkinson FL, Canfield AE, Alexander MY. Dexamethasone downregulates calcification-inhibitor molecules and accelerates osteogenic differentiation of vascular pericytes: implications for vascular calcification. Circ Res. 2006;98:1264-1272.
[13] Maas AH, van der Schouw YT, Beijerinck D, et al. Vitamin K intake and calcifications in breast arteries. Maturitas. 2007;56:273-279.
[14] Rees K, Guraewal S, Wong YL, et al. Is vitamin K consumption associated with cardio-metabolic disorders? A systematic review. Maturitas. 2010; 67:121-128.
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    Mohammad Rezaeisadrabadi, Mohammad Hossein Dashti-Rahmatabadi, Shamin Ghobadi, Fatemeh Haddad, Shokouh Taghipour Zahir, et al. (2015). Effect of Phylloquinone on Dexamethasone-Induced Calcification of Heart Muscle and Media Elastocalcinosis in Aorta Artery in Rat Model. International Journal of Clinical and Experimental Medical Sciences, 1(3), 60-64. https://doi.org/10.11648/j.ijcems.20150103.15

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    ACS Style

    Mohammad Rezaeisadrabadi; Mohammad Hossein Dashti-Rahmatabadi; Shamin Ghobadi; Fatemeh Haddad; Shokouh Taghipour Zahir, et al. Effect of Phylloquinone on Dexamethasone-Induced Calcification of Heart Muscle and Media Elastocalcinosis in Aorta Artery in Rat Model. Int. J. Clin. Exp. Med. Sci. 2015, 1(3), 60-64. doi: 10.11648/j.ijcems.20150103.15

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    AMA Style

    Mohammad Rezaeisadrabadi, Mohammad Hossein Dashti-Rahmatabadi, Shamin Ghobadi, Fatemeh Haddad, Shokouh Taghipour Zahir, et al. Effect of Phylloquinone on Dexamethasone-Induced Calcification of Heart Muscle and Media Elastocalcinosis in Aorta Artery in Rat Model. Int J Clin Exp Med Sci. 2015;1(3):60-64. doi: 10.11648/j.ijcems.20150103.15

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  • @article{10.11648/j.ijcems.20150103.15,
      author = {Mohammad Rezaeisadrabadi and Mohammad Hossein Dashti-Rahmatabadi and Shamin Ghobadi and Fatemeh Haddad and Shokouh Taghipour Zahir and Mansour Ahmadi and Mohammad Reza Lotfaliani and Aghdas Mirjalili and Ali Rezaei},
      title = {Effect of Phylloquinone on Dexamethasone-Induced Calcification of Heart Muscle and Media Elastocalcinosis in Aorta Artery in Rat Model},
      journal = {International Journal of Clinical and Experimental Medical Sciences},
      volume = {1},
      number = {3},
      pages = {60-64},
      doi = {10.11648/j.ijcems.20150103.15},
      url = {https://doi.org/10.11648/j.ijcems.20150103.15},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcems.20150103.15},
      abstract = {Background. Dexamethasone is a type of steroid medication which enhances the rate of pericyte differentiation and mineralization in vitro with concomitant suppression of calcification inhibitory molecule matrix Gla-protein (MGP). Vitamin K is an essential cofactor in the carboxylation of glutamate residues in a small group of proteins, including MGP. This study tries to assess the efficacy of vitamin K1 on dexamethasone-induced media elastocalcinosis in aorta artery and heart muscle in a rat model. Materials and Methods. 110 male rats with a normal weight range of 270 ± 20 were enrolled in this study. They received a calcification-inducing diet containing both vitamin K1 and dexamethasone during 6 or 12 weeks and were randomly assigned into two groups; a basic group (n=30), and an experimental group (n=80). The experimental group was divided into two groups receiving treatment during 6 and 12 weeks. Administration of dexamethasone was 0.5 mg/kg, intraperitoneal (IP). Vitamin K intakes were different including 5, 10, and 20 µg/kg, which were considered as low, moderate, and high intake, respectively. Results. Plasma concentrations of calcium were not affected by the different regimes and ranged between 2.27 and 2.31 millimolar (mM) (mean ± SD: 2.29 ± 0.02). According to the findings of pathologic biopsy of aorta artery and heart muscle, treatment of 0.5 mg/kg dexamethasone during 6 and 12 weeks did not induce media elastocalcinosis at all. Conclusion. Administration of 0.5 mg/kg dexamethasone during 6 and 12 weeks did not induce media elastocalcinosis at all. On the other hand, structure and histology of vessels did not change following intake of vitamin K1, therefore, different dosages of vitamin K could not affect the aorta artery status.},
     year = {2015}
    }
    

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  • TY  - JOUR
    T1  - Effect of Phylloquinone on Dexamethasone-Induced Calcification of Heart Muscle and Media Elastocalcinosis in Aorta Artery in Rat Model
    AU  - Mohammad Rezaeisadrabadi
    AU  - Mohammad Hossein Dashti-Rahmatabadi
    AU  - Shamin Ghobadi
    AU  - Fatemeh Haddad
    AU  - Shokouh Taghipour Zahir
    AU  - Mansour Ahmadi
    AU  - Mohammad Reza Lotfaliani
    AU  - Aghdas Mirjalili
    AU  - Ali Rezaei
    Y1  - 2015/09/09
    PY  - 2015
    N1  - https://doi.org/10.11648/j.ijcems.20150103.15
    DO  - 10.11648/j.ijcems.20150103.15
    T2  - International Journal of Clinical and Experimental Medical Sciences
    JF  - International Journal of Clinical and Experimental Medical Sciences
    JO  - International Journal of Clinical and Experimental Medical Sciences
    SP  - 60
    EP  - 64
    PB  - Science Publishing Group
    SN  - 2469-8032
    UR  - https://doi.org/10.11648/j.ijcems.20150103.15
    AB  - Background. Dexamethasone is a type of steroid medication which enhances the rate of pericyte differentiation and mineralization in vitro with concomitant suppression of calcification inhibitory molecule matrix Gla-protein (MGP). Vitamin K is an essential cofactor in the carboxylation of glutamate residues in a small group of proteins, including MGP. This study tries to assess the efficacy of vitamin K1 on dexamethasone-induced media elastocalcinosis in aorta artery and heart muscle in a rat model. Materials and Methods. 110 male rats with a normal weight range of 270 ± 20 were enrolled in this study. They received a calcification-inducing diet containing both vitamin K1 and dexamethasone during 6 or 12 weeks and were randomly assigned into two groups; a basic group (n=30), and an experimental group (n=80). The experimental group was divided into two groups receiving treatment during 6 and 12 weeks. Administration of dexamethasone was 0.5 mg/kg, intraperitoneal (IP). Vitamin K intakes were different including 5, 10, and 20 µg/kg, which were considered as low, moderate, and high intake, respectively. Results. Plasma concentrations of calcium were not affected by the different regimes and ranged between 2.27 and 2.31 millimolar (mM) (mean ± SD: 2.29 ± 0.02). According to the findings of pathologic biopsy of aorta artery and heart muscle, treatment of 0.5 mg/kg dexamethasone during 6 and 12 weeks did not induce media elastocalcinosis at all. Conclusion. Administration of 0.5 mg/kg dexamethasone during 6 and 12 weeks did not induce media elastocalcinosis at all. On the other hand, structure and histology of vessels did not change following intake of vitamin K1, therefore, different dosages of vitamin K could not affect the aorta artery status.
    VL  - 1
    IS  - 3
    ER  - 

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Author Information
  • Yazd Cardiovascular Research Center, Afshar Hospital, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran

  • Department of Physiology, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran

  • Shahrekord University of Medical Sciences, Shahrekord, Iran

  • Yazd Cardiovascular Research Center, Afshar Hospital, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran

  • Department of Pathology, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran

  • Department of Physiology, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran

  • Department of Food and Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran

  • Department of Histopathology, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran

  • Shahrekord University of Medical Sciences, Shahrekord, Iran

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