OBJECTIVE To investigate the effects of naringenin on the learning and memory ability of Alzheimer disease (AD) rats. METHODS 30 male SD rats were randomly divided into control group (sham operation group), model group and naringenin group. AD model was established by injecting strepoztocin (3 mg/kg) twice into each of two intracerebroventriculas. Naringenin group were given intragastric administration of naringenin once a day for 3 weeks and the other two groups were given intragadtric administration of normal saline with the same dosage and time period. After 3 weeks, learning and memory ability in all the three groups were analyzed by Morris water maze, the activity of superoxide dismutase(SOD) and the content of malondialdehyde (MDA) of the rats' brain tissue was detected by chemical colorimetric determination. Observed the expressions of Abeta42 and Abeta40 by immunohistochemical method. The expression and degree of phosphorylation of tau protein was assayed by western blotting. RESULTS 1. Compared with the sham operation group, the mean escape latency of the model group was significantly prolonged (P < 0.05) and the time that rats were in the platform quadrant was significantly shortened (P < 0.0.5). On the contrary, compared with the model group, the mean escape latency of naringenin group was significantly shortened (P < 0.05) and the time that rats were in the platform quadrant was significantly extended (P < 0.005). 2. The level of MDA in the model group, compared with the sham operation group group, was significantly increased (P < 0.05). Whereas, that of naringenin group, compared with the model group, was significantly decreased compared with the sham operation group (P < 0.05). The activity of SOD in the naringenin group was significantly increased comparing with the model group (P < 0.05). 3. The expressions of Abeta40 and Abeta42 in model group were obviously up-regulated. Instead, the expressions of Abeta40 and Abeta42 in the naringenin group were significantly down regulated. 4. There was no significant difference in the expression of tau protein among each groups. Nevertheless, the phosphorylation of tau protein in the model group was significantly enhanced than that in the control group (P < 0.05), and the phosphorylation of tau protein in the naringenin group was significantly reduced than that in the model group (P < 0.05). CONCLUSIONS Naringenin can improve learning and memory ability of model rats with Alzheimer disease through the approach of oxidative stress.