氧化应激
尼古丁
神经保护
活性氧
神经毒性
兴奋毒性
药理学
化学
甲基枸杞碱
蛋白激酶B
PI3K/AKT/mTOR通路
细胞生物学
烟碱激动剂
信号转导
烟碱乙酰胆碱受体
程序性细胞死亡
生物
神经科学
细胞凋亡
生物化学
受体
毒性
有机化学
作者
Yun Dong,Wenchuan Bi,Kai Zheng,Enni Zhu,Shaoxiang Wang,Yiping Xiong,Junlei Chang,Jianbing Jiang,Liu Bingfeng,Zhonghua Lu,Yong‐Xian Cheng
标识
DOI:10.3389/fnmol.2020.557647
摘要
Oxidative stress-induced neuronal damage has been implicated to play a dominant role in neurodegenerative disorders such as Alzheimer's disease (AD). Nicotine, a principal additive compound for tobacco users, has been demonstrated to attenuate amyloid-β-mediated neurotoxicity and NMDA-induced excitotoxicity. However, whether nicotine could protect neurons against oxidative injury remains largely unknown. In this study, the potential effects of nicotine on hydrogen peroxide (H2O2)-induced oxidative injury were investigated in a mouse hippocampal cell line (HT-22 cells). Here, we found that H2O2 resulted in cell cycle arrest at G2/M phase through excessive intracellular reactive oxygen species (ROS) generation and damaged mitochondrial functions. Importantly, nicotine at low concentrations significantly reduced intracellular ROS generation and increased cell proliferation against H2O2-induced oxidative injury. Besides, nicotine ameliorated mitochondrial dysfunction. Mechanistically, nicotine-mediated antioxidation were via specifically activating α7 nicotinic acetylcholine receptors (α7-nAChRs)/p-ERK1/2 signaling pathway rather than PI3K/Akt signaling pathway. Taken together, our findings provided an evidence for the neuroprotection of nicotine against oxidative injury, which indicates that nicotine may attenuate learning and memory injury by antioxidation in AD.
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