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Osthole promotes differentiation into neurons and reduces neuronal apoptosis via Wnt/β-catenin signaling pathway in APP transduced neural stem cells / 中国药理学通报
Chinese Pharmacological Bulletin ; (12): 1516-1523, 2015.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-480659
Biblioteca responsável: WPRO
ABSTRACT
Aim To investigate the effects of osthole ( Ost) on the ability of proliferation and differentiation in APP transduced neural stem cells( NSCs) , and neu-ronal apoptosis, in order to find related mechanism. Methods A model of Alzheimer′s disease( AD) cells was successfully established by transducing APP gene into NSCs in vitro. The ability of proliferation and dif-ferentiation was tested by staining. The viability of NSCs was determined by using CCK-8 assay. The cell apoptosis was tested by Hoechst 33258 staining. The expression of GSK-3β and β-catenin mRNA was deter-mined by RT-PCR. The expression of GSK-3β and β-catenin protein was determined by Western blot. Re-sults The ability of proliferation had increased by 10 . 24% with Ost treatment, compared with APP group. The ability of differentiation had increased by 6 . 74%with Ost treatment, compared with APP group. The vi-ability of NSCs had increased and cell apoptotic rate had decreased significantly. From the results of RT-PCR and Western blot, we could find the expression of GSK-3βmRNA and protein had decreased, and the ex-pression of β-catenin mRNA and protein had increased significantly, compared with APP group. Conclusion Ost could enhance the ability of proliferation and dif-ferentiation into more neurons of NSCs transducing APP gene, and reduce neuronal apoptosis. It might be relat-ed with activiting Wnt/β-catenin signaling pathway.

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Pharmacological Bulletin Ano de publicação: 2015 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Pharmacological Bulletin Ano de publicação: 2015 Tipo de documento: Artigo
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