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[6]‐Shogaol Attenuates Neuronal Apoptosis in Hydrogen Peroxide‐Treated Astrocytes Through the Up‐Regulation of Neurotrophic Factors
Author(s) -
Kim Sokho,
Kwon Jungkee
Publication year - 2013
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.4946
Subject(s) - oxidative stress , neurotrophin , apoptosis , neurotrophic factors , hydrogen peroxide , nerve growth factor , brain derived neurotrophic factor , reactive oxygen species , chemistry , neuroglia , microbiology and biotechnology , astrocyte , pharmacology , biology , biochemistry , neuroscience , central nervous system , receptor
Neuronal apoptosis induced by oxidative stress is a prominent feature of neurodegenerative disorders. [6]‐shogaol, a bio‐active compound in ginger, possesses potent anti‐inflammatory actions and has recently emerged as a potential therapeutic agent for neurodegenerative disorders. However, the effects of [6]‐shogaol on astroglial apoptosis following exogenously induced oxidative stress has not yet been investigated. Here, we show that the anti‐apoptotic activity of [6]‐shogaol in astrocytes following exposure to hydrogen peroxide (H 2 O 2 ) involves a marked up‐regulation of neurotrophic factors such as nerve growth factor, glial cell line‐derived neurotrophic factor, and brain‐derived neurotrophic factor. Astrocytes co‐treated with [6]‐shogaol and H 2 O 2 for 1 h showed decrease in reactive oxygen species production compared with those only treated with H 2 O 2 . Moreover, [6]‐shogaol counteracted the reduced expression of ERK1/2 in H 2 O 2 ‐treated astrocytes and protected these cells from oxidative stress and apoptosis by attenuating the impairment of mitochondrial function proteins such as Bcl‐2 and Bcl‐xL. Additionally, [6]‐shogaol inhibits the expression of the apoptotic proteins Bax and caspase‐3 in H 2 O 2 ‐treated astrocytes. This data suggest that following oxidative stress, [6]‐shogaol protects astrocytes from oxidative damage through the up‐regulating levels of neurotrophic factors. These findings provide further support for the use of [6]‐shogaol as a therapeutic agent in neurodegenerative disorders. Copyright © 2013 John Wiley & Sons, Ltd.

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