Genistein protects PC12 cells from Aβ(25-35)-induced apoptosis via JNK signaling and regulation of Fas pathway

VernacularTitle:染料木素通过JNK调控Fas通路的抗Aβ诱导的PC12细胞凋亡机制研究
Author: Jingrong CHEN ; Yaojie ZHENG ; Fuling YOU ; Hong YANG
Publication Type:Journal Article
Keywords: genistein; cell apoptosis; Aβ( 25 -35 ); JNK; Fas; mechanism
From: Chinese Pharmacological Bulletin 2015;(2):175-180
CountryChina
Language:Chinese
Abstract: 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.