PI3K/AKT/mTOR通路
自噬
蛋白激酶B
神经保护
细胞凋亡
枸杞
活性氧
药理学
化学
氧化应激
再灌注损伤
医学
缺血
内科学
生物化学
病理
替代医学
作者
Yang Yu,Xiuquan Wu,Jingnan Pu,Peng Luo,Wenke Ma,Jiu Wang,Jialiang Wei,Yuanxin Wang,Zhou Fei
标识
DOI:10.1016/j.bbrc.2017.11.165
摘要
Lycium barbarum polysaccharide (LBP) is the main active ingredient of Lycium barbarum, which exhibits several beneficial effects, including neuroprotection, anti-aging and anti-oxidation. However, the mechanism by which LBP protects against cerebral ischemia/reperfusion-induced injury remains obscure. In this study, we found that LBP pretreatment greatly attenuated oxygen glucose deprivation/reperfusion (OGD/R) injury in primary cultured hippocampal neurons. LBP also suppressed OGD/R-induced lactate dehydrogenase (LDH) leakage, and ameliorated oxidative stress. In addition, LBP significantly reduced OGD/R-induced apoptosis and autophagic cell death. LBP caused the down-regulation of cleaved Caspase-3/Caspase-3, LC3II/LC3I and Beclin 1, as well as up-regulation of Bcl-2/Bax and p62. Furthermore, mechanistic studies indicated that LBP pretreatment increased p-Akt and p-mTOR levels after OGD/R. In summary, our results indicated that LBP protects against OGD/R-induced neuronal injury in primary hippocampal neurons by activating the PI3K/Akt/mTOR signaling pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI