Salvianolic acid B, an antioxidant from Salvia miltiorrhiza, prevents Aβ25–35-induced reduction in BPRP in PC12 cells

Several lines of evidence support that β-amyloid (Aβ)-induced neurotoxicity is mediated through the generation of reactive oxygen species (ROS) and elevation of intracellular calcium. Salvianolic acid B (Sal B), the major and most active anti-oxidant from Salvia miltiorrhiza, protects diverse kinds of cells from damage caused by a variety of toxic stimuli. In the present study, we investigated the effects of Sal B against β-amyloid peptide 25–35 (Aβ25–35)-induced neurotoxicity, focused mainly on the neurotoxic effects of Aβ25–35 and the neuroprotective effects of Sal B on the expression of brain–pancreas relative protein (BPRP), which is a new protein and mainly expressed in brain and pancreas. Following exposure of PC12 cells to 20 μM Aβ25–35, a marked reduction in the expression of BPRP was observed, accompanied with decreased cell viability and increased cell apoptosis, as well as increased ROS production and calcium influx. Treatment of the PC12 cells with Sal B significantly reversed the expression of BPRP and cell viability while it decreased ROS production and intracellular calcium. These data indicate that Aβ25–35 decreases the expression of BPRP via enhanced formation of intracellular ROS and increased intracellular calcium, and that Sal B, as an anti-oxidant, protects against Aβ25–35-induced reduction in expression of BPRP through its effects on suppressing the production of ROS, calcium flux, and apoptosis. However, the role(s) of BPRP in AD and the definite mechanisms by which Sal B protects against Aβ25–35-induced reduction in the expression of BPRP require further study.