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Chinese Pharmacological Bulletin ; (12): 175-180, 2015.
Artículo en Chino | WPRIM | ID: wpr-462551

RESUMEN

Aim To investigate the effect of genistein ( GEN) against Aβ( 25 -35 )-induced PC12 cells in regulation of Fas pathway through the activation of JNK. Methods Aβ( 25 -35 )-induced PC12 cells model was established. MTT and fluorescence activated cell sorting to analyze cell viability and apoptotic rate. Fluorescence quantitative PCR was used to detect Fas apoptotic pathways related gene Fas, FasL, caspase-3 and caspase-8 mRNA relative expression. Spectropho-tometry was used to detect caspase-3 and caspase-8 en-zyme activity. Western blot was adopted to detect JNK and p-JNK protein expression level changes. Results GEN attenuated Aβ( 25-35 )-induced upregulation of Fas and FasL, caspase-3 and caspase-8 mRNA lev-el, caspase-3 and caspase-8 enzyme activity, and sig-nificantly reduced Aβ(25-35) induced JNK phospho-rylation level. Conclusion GEN can protect PC12 cells from Aβ(25-35)-induced apoptosis via reducing Aβ( 25 -35 )-induced phosphorylation of JNK activa-tion, and then inhibit the JNK dependent Fas apoptotic pathway.

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