Background: Intravenous anesthetic propofol may protect cerebral ischemic neuron through anti-apoptosis. However, research on anti-apoptosis of propofol is very rare, and its mechanism is also not definite. Objective: To observe the effect of propofol on apoptosis and necrosis rates of neuron in rats with injury of global cerebral ischemic reperfusion and the expression of genetic protein related to apoptosis and explore the protective effects of propofol on brain and its mechanism. Design: A randomized and controlled experimental study. Setting and Materials: The research was done in Beijing Neurosurgical Institute affiliated to the Capital University of Medical Sciences. Nineteen male adult Wistar rats were randomly divided into ischemic group (n=7), propofol group (n=7) and sham-operation group (n=5). Interventions: Rat models of global cerebral ischemia reperfusion were established. 1. 5 mL/hour propofol was given intravenously right after reperfusion began in propofol group, persisting 30 minutes. Brain was taken out at the time point of 24 hours of reperfusion. Apoptosis and necrosis rate and protein expression of bcl-2, Bax and p53 in hippocampal neuron of rats were detected by flow cytometry. Main outcome measures: Apoptosis rate, necrosis rate and protein expression of bcl-2, Bax and p53 in hippocampal neuron of rats. Results: Apoptosis and necrosis rate [(7.01 ± 0.79)% and( 12. 80 ± 0.92 )%] of hippocampal neuron in propofol group decreased significantly (P<0.01), as compared with ischemic group[ (10.89 ± 0.80)% and (16.67 ± 1.04)%]. Bax and p53 protein expression in propofol group [(49.93 ± 5.41)% and (10.34 ± 1.65)%] decreased significantly (P < 0.05 and P < 0.01, respectively), as compared with ischemic group [(57.05 ± 1.91)% and (13.84 ± 0.97)%], while, bcl-2 protein expression in propofol group [(9.45 ± 1.16)%] had no significant difference from that in ischemic group [(9.69 ± 0.94)%] (P > 0.05). Conclusion: Propofol can decrease apoptosis and necrosis rates of neuron in rats with global cerebral ischemic reperfusion so as to protect the brain. The mechanism may have some relationships. with decreasing the protein expression of Bax and p53, the genes promoting apoptosis.