Abstract

Aim of the study Samjunghwan (SJH) is a multi-herbal traditional medicine composed of Mori Fructus, Lycii Radicis Cortex, and Atractylodis Rhizoma Alba and it is clinically applied as an anti-aging agent in neurodegenerative disorders, to promote longevity. In the present study, we evaluated the neuroprotective effect of SJH in Alzheimer's disease induced by amyloid-beta (Abeta) and examined the related pathways. Materials and methods To evaluate the protective effect of SJH, we conducted thiazolyl blue tetrazolium bromide, lactate dehydrogenase, and MAP-2 staining assays of primary cultured rat cortical neurons stressed by Abeta 25–35. To investigate the possible mechanism of action, we examined the Bcl-2/Bax expression ratio, mitochondrial membrane potential (Δ ψ M ), cytochrome C release, and caspase-3 activation, focusing on the mitochondria-mediated apoptotic pathways. Results SJH at concentrations of 10 and 100 μg/ml provided significant protection of rat cortical neurons from Abeta 25–35 neurotoxicity. At the maximum effective dose of 100 μg/ml, SJH significantly increased the anti-apoptotic protein (Bcl-2)/pro-apoptotic protein (Bax) ratio and inhibited Δ ψ M depolarization, cytosolic cytochrome C release, and caspase-3 activation. Conclusion SJH appears to provide neuroprotection against mitochondria-mediated apoptotic pathways in this Abeta 25–35-induced Alzheimer's disease model.

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