Arctigenin (
Arc) has been shown to act on
scopolamine-induced
memory deficit mice and to provide a
neuroprotective effect on cultured cortical neurons from
glutamate-induced neurodegeneration through mechanisms not completely defined. Here, we investigated the
neuroprotective effect of
Arc on H89-induced cell damage and its potential mechanisms in mouse cortical neurons and human SH-SY5Y
neuroblastoma cells. We found that
Arc prevented cell viability loss induced by
H89 in human SH-SY5Y cells. Moreover,
Arc reduced intracellular
beta amyloid (Aβ) production induced by
H89 in neurons and human SH-SY5Y cells, and
Arc also inhibited the
presenilin 1(PS1)
protein level in neurons. In addition, neural apoptosis in both types of cells, inhibition of neurite outgrowth in human SH-SY5Y cells and reduction of synaptic marker
synaptophysin (SYN) expression in neurons were also observed after
H89 exposure. All these effects induced by
H89 were markedly reversed by
Arc treatment.
Arc also significantly attenuated downregulation of the phosphorylation of CREB (p-CREB) induced by
H89, which may contribute to the
neuroprotective effects of
Arc. These results demonstrated that
Arc exerted the ability to protect neurons and SH-SY5Y cells against H89-induced cell injury via upregulation of p-CREB.