Journal
JOURNAL OF PHARMACY AND PHARMACOLOGY
Volume 65, Issue 12, Pages 1736-1744Publisher
WILEY
DOI: 10.1111/jphp.12096
Keywords
-amyloid peptide; apoptosis; dicaffeoylquinic acids; lipid peroxidation; nicotinic acetylcholine receptor
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Funding
- Chinese National Natural Science Foundation [81260317]
- Foundation in the Ministry of Science and Technology of China [2013DAI05B03, 2010DFB30530]
- Foundation in Guizhou Province
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ObjectivesThis 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 -amyloid peptide (A(25-35)). MethodsThe neuroblastoma SH-SY5Y cell line was treated with A 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 3 and 7 nicotinic acetylcholine receptor (nAChR) subunit proteins by Western blotting. Key findingsWhen the cells were exposed to A(25-35), MTT reduction declined, oxidative stress and apoptosis were enhanced, and the expression of 3 and 7 nAChR subunit proteins was lowered. Expression of the 7 nAChR subunit protein was increased by all three diCQAs, and the level of 3 was increased by 3, 5-diCQA and 4, 5-diCQA. Significantly, pretreatment with diCQAs attenuated the neurotoxic effects of A(25-35), a neuroprotective effect in which the upregulation of 7 and 3 nAChR may be involved. ConclusionThe diCQAs exert a protective effect on A-induced neurotoxicity in SH-SY5Y cells and a potential underlying mechanism involving stimulation of nAChRs.
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