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Neuroprotective effects of 3,5‐dicaffeoylquinic acid on hydrogen peroxide‐induced cell death in SH‐SY5Y cells
Author(s) -
Kim SungSoo,
Park RanYoung,
Jeon HyunJung,
Kwon YongSoo,
Chun Wanjoo
Publication year - 2005
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.1652
Subject(s) - neuroprotection , oxidative stress , sh sy5y , glutathione , hydrogen peroxide , pharmacology , intracellular , programmed cell death , apoptosis , chemistry , biochemistry , biology , cell culture , enzyme , genetics , neuroblastoma
Oxidative stress plays an important role in the pathological processes of a variety of neurodegenerative diseases. The neuroprotective effects of 3,5‐diCQA and 3,4‐diCQA, two caffeoylquinic acid derivatives present in Dipsacus asper , on hydrogen peroxide (H 2 O 2 )‐induced neuronal cell damage were evaluated in this study. SH‐SY5Y cells treated with H 2 O 2 exhibited a decrease in survival and intracellular glutathione and also an increase in the caspase‐3 activity. However, pretreatment of cells with 3,5‐diCQA attenuated the neuronal death and caspase‐3 activation induced by H 2 O 2 . In addition, 3,5‐diCQA restored H 2 O 2 ‐induced depletion of intracellular glutathione. 3,5‐diCQA showed significant protective effects although it could not completely suppress H 2 O 2 ‐induced cell injury to control levels. The data suggest that 3,5‐diCQA might be a potential therapeutic agent for treating or preventing neurodegenerative diseases implicated with oxidative stress. Copyright © 2005 John Wiley & Sons, Ltd.
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