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Chinese Journal of Pathology ; (12): 116-120, 2013.
Article Dans Chinois | WPRIM | ID: wpr-256241

Résumé

<p><b>OBJECTIVE</b>To investigate the effects of α3 neuronal nicotinic acetylcholine receptor (nAChR) on apoptosis and p38 signal transduction pathway in SH-SY5Y cells and to assess the roles of α3 nAChR in the pathogenesis of Alzheimer's disease (AD).</p><p><b>METHODS</b>The levels of α3 nAChR mRNA and protein were measured by real-time PCR and Western blot, respectively, in SH-SY5Y cells transfected with α3 nAChR siRNA. The mRNA level of bcl-2 and bax was measured by the real-time PCR. The siRNA transfected SH-SY5Y cells and control were then treated with 10 µmol/L Aβ25-35 for another 48 h, and the change in apoptotic rate and the levels of p-p38 and p38 were measured by flow cytometry and Western blot. Subsequently these SH-SY5Y cells were exposed to a blocker of p38 protein, and the apoptotic rate was measured again.</p><p><b>RESULTS</b>Compared to the controls, the expression of α3 nAChR at mRNA and protein levels in the SH-SY5Y cells transfected with α3 nAChR siRNA decreased by 95% and 86%, respectively; the mRNA levels of bax increased 2.11 times and that for bcl-2 decreased 0.53 times. The apoptotic rate was unaffected (3.40% ± 0.20%); but it increased after Aβ25-35 treatment (24.52% ± 1.59%); the level of p-p38 protein also increased by 178% in the α3 nAChR inhibited cells treated with Aβ25-35. Compared to controls, the Aβ25-35-treated SH-SY5Y cells and the Aβ25-35-treated and siRNA-transfected cells both showed a reduction in apoptosis after treatment with p38 blocker, especially in the former.</p><p><b>CONCLUSION</b>The siRNA silencing of α3 nAChR mRNA may enhance the effect of Aβ25-35 on the cell apoptosis by increasing the levels of p38 protein and bax mRNA and decreasing the level of bcl-2 mRNA, which may play a role in the pathogenesis of AD.</p>


Sujets)
Humains , Maladie d'Alzheimer , Peptides bêta-amyloïdes , Métabolisme , Apoptose , Lignée cellulaire tumorale , Extinction de l'expression des gènes , Neuroblastome , Métabolisme , Anatomopathologie , Fragments peptidiques , Métabolisme , Protéines proto-oncogènes c-bcl-2 , Génétique , Métabolisme , ARN messager , Métabolisme , Petit ARN interférent , Génétique , Récepteurs nicotiniques , Génétique , Métabolisme , Transduction du signal , Transfection , Protéine Bax , Génétique , Métabolisme , p38 Mitogen-Activated Protein Kinases , Métabolisme
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