机构：[1]Laboratory of Ethnopharmacology, Regenerative Medicine Research Center, West China Hospital, West China Medical School, and Institute for Nanobiomedical Technology and Membrane Biology, Sichuan University, No. 1 Keyuansilu, Gaopeng Dadao, Chengdu, Sichuan 610041, People’s Republic of China四川大学华西医院[2]Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of China[3]Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of China[4]State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of China
Magnolol, an orally available compound from Magnolia officinalis used widely in traditional herbal medicine against a variety of neuronal diseases, possesses potent antioxidant properties and protects the brain against oxidative damage. The aim of the work is to examine the protective mechanisms of magnolol on human neuroblastoma SH-SY5Y cells against apoptosis induced by the neurotoxin acrolein, which can cause neurodegenerative disorders by inducing oxidative stress. By investigating the effect of magnolol on neural cell damage induced by the neurotoxin acrolein, we found that magnolol pretreatment significantly attenuated acrolein-induced oxidative stress through inhibiting reactive oxygen species accumulation caused by intracellular glutathione depletion and nicotinamide adenine dinucleotide phosphate oxidase activation. We next examined the signaling cascade(s) involved in magnolol-mediated antiapoptotic effects. The results showed that acrolein induced SH-SY5Y cell apoptosis by activating mitochondria/caspase and MEK/ERK signaling pathways. Our findings provide the first evidence that magnolol protects SH-SY5Y cells against acrolein-induced oxidative stress and prolongs SH-SY5Y cell survival through regulating JNK/mitochondria/caspase, PI3K/MEK/ERK, and PI3K/Akt/FoxO1 signaling pathways.
基金：
China National
“12.5” Foundation (no. 2011BAJ07B04) and the Open Foundation
(SKLODSCUKF2012-04) from the State Key Laboratory of Oral
Diseases, Sichuan University for the financial support and National
Natural Science Foundation of China (no. 20972105 and 20772087)
and Sichuan Province Foundation (no. 2008SZ0024).
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2013]版：
大类|3 区医学
小类|4 区生化与分子生物学4 区神经科学
最新[2023]版：
大类|4 区医学
小类|4 区生化与分子生物学4 区神经科学
第一作者：
第一作者机构：[1]Laboratory of Ethnopharmacology, Regenerative Medicine Research Center, West China Hospital, West China Medical School, and Institute for Nanobiomedical Technology and Membrane Biology, Sichuan University, No. 1 Keyuansilu, Gaopeng Dadao, Chengdu, Sichuan 610041, People’s Republic of China[2]Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan 610041, People’s Republic of China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Dong Liqun,Zhou Shu,Yang Xiaohua,et al.Magnolol protects against oxidative stress-mediated neural cell damage by modulating mitochondrial dysfunction and PI3K/Akt signaling.[J].Journal of molecular neuroscience : MN.2013,50(3):469-81.doi:10.1007/s12031-013-9964-0.
APA：
Dong Liqun,Zhou Shu,Yang Xiaohua,Chen Qianming,He Yang&Huang Wen.(2013).Magnolol protects against oxidative stress-mediated neural cell damage by modulating mitochondrial dysfunction and PI3K/Akt signaling..Journal of molecular neuroscience : MN,50,(3)
MLA：
Dong Liqun,et al."Magnolol protects against oxidative stress-mediated neural cell damage by modulating mitochondrial dysfunction and PI3K/Akt signaling.".Journal of molecular neuroscience : MN 50..3(2013):469-81
