Schisandrin B protects rat cortical neurons against Aβ1-42-induced neurotoxicity

In the present study, we investigated the neuroprotective effects of schisandrin B on amyloid-beta(1-42)-induced toxicity and its potential mechanisms in rat cortical neuron cells. Amyloid beta(1-42) significantly reduced cell viability and increased apoptosis. Pretreatment with schisandrin B prior to amyloid-beta(1-42) exposure significantly elevated cell viability and reduced apoptosis. The anti-apoptotic effect of schisandrin B in rat cortical neurons was mediated by up-regulation of the anti-apoptotic protein Bcl-2 and down-regulation of the pro-apoptotic protein Bax. Schisandrin B also reduced the release of mitochondrial cytochrome c into cytosol and decreased caspase-9 and caspase-3 activities. Furthermore, schisandrin B increased activities of anti-oxidant reduced glutathione and decreased production of oxidative glutathione. Taken together, these results suggest that schisandrin B protected primary cultures of rat cortical cells against amyloid-beta(1-42)-induced neurotoxicity through anti-apoptosis involved in a mitochondria-mediated pathway and anti-oxidant action. Schisandrin B may represent a potential treatment strategy for Alzheimer's disease.