The Inhibitory Effects of Ahnjeonbaekho-tang on FRTL-5 Cell Proliferation and Thyroxine Synthesis

  • Kang, Shin-Ik (Deptartment of Internal medicine, College of Oriental Medicine, Kyung Hee University) ;
  • Lee, Byung-Cheol (Deptartment of Internal medicine, College of Oriental Medicine, Kyung Hee University) ;
  • Ahn, Young-Min (Deptartment of Internal medicine, College of Oriental Medicine, Kyung Hee University) ;
  • Doo, Ho-Kyung (Deptartment of Internal medicine, College of Oriental Medicine, Kyung Hee University) ;
  • Ahn, Se-Young (Deptartment of Internal medicine, College of Oriental Medicine, Kyung Hee University)
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  • 안세영 (경희의료원 부속한방병원)
  • Published : 2006.09.30

Abstract

Objective : Graves' disease, the most common cause of hyperthyroidism, is an autoimmune disorder associated with autoantibodies to the TSH receptor. The clinical features of Graves' disease are goiter and hypermetabolic symptoms induced by excessive hormones. Antithyroid drug therapy is the first-line treatment for Graves' disease in Korea, Japan and European countries. Yet in spite of a long period and high-dose of treatment, it is hard to achieve remission because of adverse effects, frequent recurrence and resistance to antithyroid drugs. Recently, it has been reported that the abnormal thyroid hormone and clinical symptoms of Graves' disease were reduced by Ahnjeonbaekho-tang (AJBHT). Methods : To investigate the effectiveness and action mechanism of AJBHT, we studied the influence of AJBHT on FRTL-5 thyroid cell proliferation, DNA synthesis and expression of T4, TSH, cAMP, Tg and TPO mRNA. Results : AJBHT significantly inhibited the FRTL-5 cell proliferation, DNA synthesis, T4 synthesis, cAMP production and the expression of Tg mRNA in comparison with control and MMI. Conclusions : These results suggest that AJBHT may inhibit the cell proliferation and DNA synthesis by regulating the cAMP, and suppress the T4 synthesis by modulating Tg mRNA expression and cAMP synthesis, and that it may be useful agent for treating the goiter and hormone abnormality of Graves' disease.

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