Objective To evaluate the effect of aminoguanidine (AG) on neuronal apoptosis induced by focal cerebral ischemia in rats and the possible mechanism of protective effect of AG against cerebral ischemic injury.Methods Fifty-four male SD rats weighing 250-290 g were randomly divided into 3 groups: (1) sham operated group (SH group, n = 18); (2) ischemic group (IS group, n = 18) and (3) AG group(n = 18). SH, IS and AG groups were further divided into 3 subgroups according to the administration time:2, 6 or 12 h following cerebral ischemia. In AG group AG 100 mg? kg-1 was given intraperitoneally twice a day for 3 consecutive days. In IS group normal saline was given instead of AG. Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO). A nylon thread with rounded tip which was inserted into left internal carotid artery cranially until resistance was felt. The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm. Focal cerebral ischemia was confirmed by left Homer's syndrome and right side hemiplegia. In SH group the carotid artery was exposed but no thread was inserted. The nylon thread was with drawn to allow reperfusion after 2, 6 or 12 h MCAO. The animals were detected by flow cytometry. Results Significantly increased DNA fragmentation indicative of apoptosis was detected after MCAO. The percentage of apoptotic cells and expression of Bax protein were significantly lower after 2, 6 and 12 h ischemia in AG group than in IS group but still significantly higher than in SH group. The expression of Bcl-2 protein was significantly higher after 2,6 and 12 h in AG group than in IS group. There was no significant difference in the expression of Bcl-2 protein between IS and SH group. Conclusion AG can protect neurons from apoptosis through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression.