Registro completo |
Provedor de dados: |
BJMBR
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País: |
Brazil
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Título: |
Effect of iodide on Fas, Fas-ligand and Bcl-w mRNA expression in thyroid of NOD mice pretreated with methimazole
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Autores: |
Boechat,L.H.B.
Vilella,C.A.
Zollner,R.L.
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Data: |
2002-03-01
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Ano: |
2002
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Palavras-chave: |
Thyroiditis
Nonobese diabetic mice
Apoptosis
Methimazole
Iodide
Fas mRNA
Fas-L mRNA
Bcl-w mRNA
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Resumo: |
Nonobese diabetic (NOD) mice and a derived strain, NOD.H.2h4, have been used as a model for experimental spontaneous thyroiditis and thyroiditis induced by iodide excess after a goiter-inducing period. Some authors have proposed that iodide, given after methimazole or propylthiouracil, is capable of inducing apoptosis in thyroid cells and that anti-thyroid drugs can modulate the expression of apoptosis components such as Fas and its ligand (Fas-L). Here we evaluated the effect of potassium iodide (20 µg/animal for 4 days, ip) given to NOD mice at the 10th week of life after exposure to methimazole (1 mg/ml) in drinking water from the 4th to the 10th week of life. Fas, Fas-L and Bcl-w expression were analyzed semiquantitatively by RT-PCR immediately after potassium iodide administration (group MI44D) or at week 32 (MI32S). Control groups were added at 10 (C10) and 32 weeks (C32), as well as a group that received only methimazole (CM10). An increase in the expression of Fas-L and Bcl-w (P<0.01, ANOVA) was observed in animals of group MI44D, while Fas was expressed at higher levels (P = 0.02) in group C32 (72.89 ± 47.09 arbitrary units) when compared to group C10 (10.8 ± 8.55 arbitrary units). Thus, the analysis of Fas-L and Bcl-w expression in the MI44D group and Fas in group C32 allowed us to detect two different patterns of expression of these apoptosis components in thyroid tissue of NOD mice.
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Tipo: |
Info:eu-repo/semantics/article
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Idioma: |
Inglês
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Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2002000300003
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Editor: |
Associação Brasileira de Divulgação Científica
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Relação: |
10.1590/S0100-879X2002000300003
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Formato: |
text/html
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Fonte: |
Brazilian Journal of Medical and Biological Research v.35 n.3 2002
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Direitos: |
info:eu-repo/semantics/openAccess
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