神经毒性
细胞凋亡
蛋白激酶B
PI3K/AKT/mTOR通路
LY294002型
化学
细胞色素c
药理学
程序性细胞死亡
胞浆
β淀粉样蛋白
细胞生物学
癌症研究
医学
生物化学
生物
毒性
有机化学
酶
肽
作者
Huixue Zhang,Yuze Cao,Lixia Chen,Jianjian Wang,Qinghua Tian,Ning Wang,Zhaojun Liu,Jie Li,Na Wang,Xiaokun Wang,Piyun Sun,Lihua Wang
标识
DOI:10.1016/j.carbpol.2014.10.034
摘要
One of the pathological hallmarks of Alzheimer's disease (AD) is the progressive accumulation of beta-amyloid (Aβ) in the form of senile plaques, and Aβ induced neurotoxicity has been identified as a major cause of the onset of AD. In this study, we investigated the protective effects of a polysaccharide (PS-WNP) from Polygonatum sibiricum against the Aβ25–35-induced neurotoxicity in PC12 cells and explored the underlying mechanism. The results showed that pretreatment with PS-WNP significantly attenuated cell death and the elevated Bax/Bcl-2 ratio evoked by Aβ25–35, and subsequently inhibited mitochondrial dysfunction and cytochrome c release into the cytosol. Moreover, PS-WNP significantly inhibited Aβ25–35 induced caspase-3 activation and enhanced the protein levels of phosphorylated Akt (p-Akt) in PC12 cells. Additionally, pretreatment with the PI3K inhibitor (LY294002) completely abolished the protective effects of PS-WNP against Aβ25–35-induced neuronal cell apoptosis. These observations unambiguously suggested that the protective effect of PS-WNP against Aβ25–35-induced apoptosis in PC12 cells was associated with the enhancement of PI3K/Akt signaling pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI