Pretreatment of SH-SY5Y cells with dicaffeoylquinic acids attenuates the reduced expression of nicotinic receptors, elevated level of oxidative stress and enhanced apoptosis caused by [beta]-amyloid peptide

Objectives This in vitro investigation was designed to examine potential neuroprotection by dicaffeoylquinic acids (diCQAs) extracted from a traditional Chinese medicinal herb herba erigerontis and their effects against the toxicity induced by [beta]-amyloid peptide (A[beta]25-35). Methods The neuro...

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Published in:Journal of pharmacy and pharmacology 2013-12, Vol.65 (12), p.1736
Main Authors: Deng, Jie, Qi, Xiao-Lan, Guan, Zhi-Zhong, Yan, Xiu-Ming, Huang, Yong, Wang, Yong-Lin
Format: Article
Language:English
Subjects:
Acids
Apoptosis
Medical research
Oxidative stress
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Summary:Objectives This in vitro investigation was designed to examine potential neuroprotection by dicaffeoylquinic acids (diCQAs) extracted from a traditional Chinese medicinal herb herba erigerontis and their effects against the toxicity induced by [beta]-amyloid peptide (A[beta]25-35). Methods The neuroblastoma SH-SY5Y cell line was treated with A[beta] or 3, 4-diCQA, 3, 5-diCQA or 4, 5-diCQA. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) reduction was assayed by spectrophotometrical method, lipid peroxidation (malondialdehyde) on the basis of the level of thiobarbituric acid-reactive substance, the activity of superoxide dismutase by the xanthine oxidase procedure, the frequency of apoptosis by flow cytometry, and the levels of [alpha]3 and [alpha]7 nicotinic acetylcholine receptor (nAChR) subunit proteins by Western blotting. Key findings When the cells were exposed to A[beta]25-35, MTT reduction declined, oxidative stress and apoptosis were enhanced, and the expression of [alpha]3 and [alpha]7 nAChR subunit proteins was lowered. Expression of the [alpha]7 nAChR subunit protein was increased by all three diCQAs, and the level of [alpha]3 was increased by 3, 5-diCQA and 4, 5-diCQA. Significantly, pretreatment with diCQAs attenuated the neurotoxic effects of A[beta]25-35, a neuroprotective effect in which the upregulation of [alpha]7 and [alpha]3 nAChR may be involved. Conclusion The diCQAs exert a protective effect on A[beta]-induced neurotoxicity in SH-SY5Y cells and a potential underlying mechanism involving stimulation of nAChRs. [PUBLICATION ABSTRACT]
ISSN:0022-3573
2042-7158
DOI:10.1111/jphp.12096