Neuroprotection against Aβ25-35-induced apoptosis by Salvia miltiorrhiza extract in SH-SY5Y cells

The neurotoxicity of beta-amyloid protein (A beta) contributes significantly to the pathogenesis of Alzheimer's disease (AD), and hence the attractive therapeutic strategies focusing on the modulation of A beta-induced neurotoxicity are warranted. The present study aims to investigate the neuroprotection and underlying mechanisms by which Salvia miltiorrhiza Bunge (Lamiaceae) extract (SME) protects against A beta(25-35)-induced apoptosis in SH-SY5Y cells. 2 h Pre-treatment of SH-SY5Y cells with SME (0.01, 0.1 or 0.2 mg raw herb/ml) concentration-dependently attenuated A beta(25-35)-induced cell death, as evidenced by the increase in cell viability and decrease in neuronal apoptosis. In addition, SME suppressed the increased intracellular reactive oxygen species levels, decreased the protein expression of cleaved caspase-3, cytosolic cytochrome c, and Bax/Bcl-2 ratio. These findings taken together suggest that SME provides substantial neuroprotection against A beta(25-35)-induced neurotoxicity in SH-SY5Y cells, at least in part, via inhibiting oxidative stress and attenuating the mitochondria-dependent apoptotic pathway. The approach used in this study may also be useful for the screening of therapeutic agents for AD and other related neurodegenerative disease. (C) 2014 Elsevier Ltd. All rights reserved.