Role of Notch-1 signaling pathway in PC12 cell apoptosis induced by amyloid beta-peptide （25-35）

• Published in: 中国神经再生研究：英文版 2014, Vol.9 (13), p.1297-1302
• Main Author: Huimin Liang Yaozhou Zhang Xiaoyan Shi Tianxiang Wei Jiyu Lou
• Format: Article
• Language: English
• Subjects: PC12细胞; 信号通路; 淀粉样蛋白; 甘氨酸叔丁酯; 细胞凋亡; 胱天蛋白酶-3; 诱导; 超氧化物歧化酶
• ISSN: 1673-5374

Recent studies have demonstrated that Notch-1 expression is increased in the hippocampus of Alzheimer＇s disease patients. We speculate that Notch-1 signaling may be involved in PC12 cell apoptosis induced by amyloid beta-peptide （25-35） （Aβ25-35）. In the present study, PC12 cells were cultured with different doses （0, 0.1, 1.0, 10 and 100 nmol/L） of N-[N-（3,5-Difluorophenacetyl）-L-alanyl]-S-phenylglycine t-butyl ester, a Notch-1 signaling pathway inhibitor, for 30 minutes. Then cultured cells were induced with Aβ25-3s for 48 hours. Pretreatment of PC12 cells with high doses of N-[N-（3,5-Difluorophenacetyl）-L-alanyl]-S-phenylglycine t-butyl ester （〉 10 nmol/L） prolonged the survival of PC12 cells after Aβ25-35 induction, decreased the expression of apoptosis-related proteins caspase-3, -8, -9, increased the activity of oxidative stress-related superoxide dismutase and catalase, inhibited the production of active oxygen, and reduced nuclear factor kappa B expression. This study indicates that the Notch-1 signaling pathway plays a pivotal role in Aβ25-35-induced PC12 apoptosis.