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 β-amyloid peptide

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.