To investigate the effects of diazoxide (ATPsensitive potassium channel opener) and cyclosporine A and their combination on apoptosis induced by betaAmyloid protein (Aβ142) on cultured primitive rat basal forebrain cholinergic neurons. MethodsThe cell apoptosis model was induced by Aβ142(2?μmmol/L), and then 500?μmol/L diazoxide, 20?μmol/L cyclosporine A and their combination were used to interfere with it. Cell morphology was observed by an inverted microscope,changes of cell apoptosis were determined by MTT, and expressions of target proteins (bcl2, bax, cytochrome C, caspasce3 and Cleaved Caspase3) were determined by Western blot when the neurons were interfered with by the drugs for different times (24, 72?h). Results ① Being exposed to Aβ142 for 72?h, cell activity remarkably decreased(P<0.001), expression of Bcl2 decreased (P<0.01) and expressions of cytochrome C, caspasce3 and Cleaved Caspase3 increased(P<0.01, P<0.001, P<0.01). Expression of Bax had no change but the value of Bcl2/Bax decreased(P<0.01). ② Expression of Bcl2 increased when the cell apoptosis model was exposed to diazoxide, cyclosporine A and their combination for 24?h(P<0.05, P<0.01, P<0.01). When the cell apoptosis model was exposed to diazoxide, cyclosporine A and their combination for 72?h, expression of Bcl2 obviously increased (P<0.05, P<0.01, P<0.001), expressions of Cytochrome C, Caspasce3 and Cleaved Caspase3 decreased(P<0.05, P<0.01, P<0.001), and cell activity increased(P<0.01, P<0.001). ConclusionBeing exposed to Aβ142 for 72?h, neuron apoptosis occurs. Diazoxide and cyclosporine A and their combination could protect neurons from apoptosis induced by Aβ142.