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Provedor de dados:  BJMBR
País:  Brazil
Título:  Lipopolysaccharide-induced dental pulp cell apoptosis and the expression of Bax and Bcl-2 in vitro
Autores:  Yang,H.
Zhu,Y.T.
Cheng,R.
Shao,M.Y.
Fu,Z.S.
Cheng,L.
Wang,F.M.
Hu,T.
Data:  2010-11-01
Ano:  2010
Palavras-chave:  Dental pulp cells
Lipopolysaccharide
Apoptosis
Bax
Bcl-2
Resumo:  Lipopolysaccharide exerts many effects on many cell lines, including cytokine secretion, and cell apoptosis and necrosis. We investigated the in vitro effects of lipopolysaccharide on apoptosis of cultured human dental pulp cells and the expression of Bcl-2 and Bax. Dental pulp cells showed morphologies typical of apoptosis after exposure to lipopolysaccharide. Flow cytometry showed that the rate of apoptosis of human dental pulp cells increased with increasing lipopolysaccharide concentration. Compared with controls, lipopolysaccharide promoted pulp cell apoptosis (P < 0.05) from 0.1 to 100 μg/mL but not at 0.01 μg/mL. Cell apoptosis was statistically higher after exposure to lipopolysaccharide for 3 days compared with 1 day, but no difference was observed between 3 and 5 days. Immunohistochemistry showed that expression of Bax and Bcl-2 was enhanced by lipopolysaccharide at high concentrations, but no evident expression was observed at low concentrations (0.01 and 0.1 μg/mL) or in the control groups. In conclusion, lipopolysaccharide induced dental pulp cell apoptosis in a dose-dependent manner, but apoptosis did not increase with treatment duration. The expression of the apoptosis regulatory proteins Bax and Bcl-2 was also up-regulated in pulp cells after exposure to a high concentration of lipopolysaccharide.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2010001100003
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X2010007500102
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.43 n.11 2010
Direitos:  info:eu-repo/semantics/openAccess
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