Previous studies reported that upregulating the expression of Bcl-2 can protect neuronal cells from apoptosis (43), and that decreased Bax or increased Bcl-2 indicate anti-apoptotic neuroprotective effects in a rat model of VaD (44), while the activity of c-Jun was found to be increased in rats with cerebral ischemia/reperfusion (45), which was in accordance with the results of the present study. This evidence concerns the gene JUN and brain ischemia.