Co-treatment with the seed of Carthamus tinctorius L. and the aerial part of Taraxacum coreanum synergistically suppresses Aβ25-35-induced neurotoxicity by altering APP processing

Abstract

Accumulation of beta-amyloid peptide (A beta) induces neurotoxicity, which is the primary risk factor in the pathogenesis of Alzheimer's disease (AD). The cleavage of amyloid precursor protein (APP) by the beta- (BACE) and gamma- (PS1, PS2) secretases is a critical step in the amyloidogenic pathway. The induction of neuronal apoptosis by A beta involves increased expression of B-cell lymphoma protein 2 (Bcl-2)-associated X (Bax) and decreased Bcl-2 expression. The seed of Carthamus tinctorius L. (CTS) and the aerial part of Taraxacum coreanum (TC) are traditional herbs used to treat several neurodegenerative diseases. In this study, the neuroprotective effects of co-treatment with CTS and TC on A beta-induced neurotoxicity in SH-SY5Y neuroblastoma cells and the underlying mechanisms were investigated. CTS, TC, and the co-treatment (CTS + TC) were added to A beta 25-35-treated SH-SY5Y cells. CTS + TC synergistically increased cell viability and inhibited reactive oxygen species production. CTS + TC resulted in significant downregulation of BACE, PS1, PS2, and APP, as well as the 99-aa C-terminal domain of APP, compared with either CTS or TC alone. Compared with the single herbs, co-treatment with CTS and TC markedly decreased the expression of Bax and increased the expression of Bcl-2, consistent with its anti-apoptotic effects. These findings suggest that co-treatment with CTS and TC may be useful for AD prevention.