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J Mol Neurosci. 2013 Jul;50(3):469-81. doi: 10.1007/s12031-013-9964-0. Epub 2013 Feb 14.

Magnolol protects against oxidative stress-mediated neural cell damage by modulating mitochondrial dysfunction and PI3K/Akt signaling.

Author information

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.

Abstract

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.

PMID:
23404573
DOI:
10.1007/s12031-013-9964-0
[Indexed for MEDLINE]

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