Cardiac up-regulation of apolipoprotein D in a rat model of hypo- and hyperthyroidism

Authors

  • Pakdel, Abbas Department of Biochemistry, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran-Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran
  • Pakdel, Roghayeh Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran
  • Salami , Marziyeh Department of Biochemistry, Faculty of Medicine, Semnan University of Medical Sciences, Semnan, Iran-Student Research Committee, Semnan University of Medical Sciences, Semnan, Iran
  • Sameni, Hamidreza Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran
  • Vafaei , Abbas Ali Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran
Abstract:

Introduction: Cardiac tissue is one of the organs affected by thyroid hormones imbalances. Apolipoprotein D is a multifunctional glycoprotein that is expressed in various tissues including heart tissue. The aim of this study was to evaluate the effect of both hypothyroidism and hyperthyroidism on the level of apolipoprotein D protein in the heart tissue. Materials and Methods: In order to induce hypothyroidism and hyperthyroidism in white mice, propylthiouracil (PTU, 100 ppm) and levothyroxine (L-T4, 8 ppm) dissolved in water  and were used for 6 weeks, respectively. ELISA method was used to measure the total T3 hormone in rat serum. After confirming the model, the mice were anesthetized and the heart tissue was removed and the ventricle and apex of the heart were used for histological examination. Immunohistochemistry was used to evaluate the expression level of apolipoprotein D. Results: We showed for the first time that the expression of apolipoprotein D in the hearts of hypothyroid (P<0.05) and hyperthyroid (P<0.001) rats increased significantly compared to the control group. Conclusion: It is suggested that the increase in cardiac apolipoprotein D levels due to thyroid disorders may be part of an inherent system to protect the heart against damage caused by oxidative stress and inflammation in these disorders.  

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volume 23  issue 3

pages  409- 414

publication date 2021-05

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