BACKGROUND: Studies have shown that the Rubus parvifolius L. (RP) plant extract exhibits protective effects on cerebral ischemia. This effect is reflected in altered ischemic neuronal apoptosis and associated protein expression. OBJECTIVE: To explore the neuroprotective mechanism of RP after cerebral ischemia injury. DESIGN, TIME AND SETTING: Randomized control experiment of cellular, molecular, and protein levels. The experiment was completed at Chongqing Medical University at the School of Pharmacy Laboratories and Basic Medical Institute from October 2005 to January 2006. MATERIALS: Twenty-four adult, male, Wistar rats, weighing (28 ± 20) g. RP extract, which was a product of ethanol extraction, was provided by the Laboratory of Pharmaceutical Analysis, Chongqing Medical University. RP was dissolved in distilled water to a concentration of 10 mg/mL. All rats were randomly assigned into four groups: 5 g/kg RP, 10 g/kg RP, model, and sham-surgery, with 6 rats in each group. METHODS: In the 5 and 10 g/kg RP groups, as well as the model group, the middle cerebral artery was occluded (MCAO) for 60 minutes, resulting in focal cerebral ischemia, followed by reperfusion for 24 hours. Rats in the 5 and 10 g/kg RP groups received 5 and 10 g/kg RP, respectively. The RP treatment group received RP intragastrically (once a day) for 3 days. One hour after the last dose, rats were subjected to MCAO. The same surgical procedure was performed in the sham-surgery group, except the suture was introduced into the external carotid artery, but not advanced. Rats in the model group were subjected to MCAO. The sham-surgery and model groups received intragastrically administered normal saline once per day for 3 days. One hour after the last dose, the rats were subjected to surgery. MAIN OUTCOME MEASURES: TUNEL labeling and immunohistochemical methods were used to in- vestigate changes in neuronal apoptosis and expression of the apoptosis-related proteins, Bax and Bcl-2, on the ischemic hemisphere, as well as the contralateral hemisphere, after administration of RP or normal saline. RESULTS: All 24 Wistar rats were included in the final analysis, without any loss. Compared with the sham-surgery group, the number of the TUNEL-positive cells in the model group, as well as the 5 and 10 g/kg RP treatment groups, were significantly increased in the ischemic hemisphere (P < 0.05). Compared with the sham-surgery group, the number of Bcl-2-positive and Bax-positive cells increased significantly in the model group (P < 0.01). The number of Bcl-2-positive cells increased, and the number of Bax-positive cells decreased in the model group, compared to the 5 and 10 g/kg RP treatment groups (P < 0.05-0.01). CONCLUSION: RP can prevent neuronal apoptosis following cerebral ischemic-reperfusion of rats. The mechanism underlying the RP-induced neuroprotection in the cerebral ischemia injury may be related to increased Bcl-2 expression and decreased Bax expression. BACKGROUND: Studies have shown that the Rubus parvifolius L. (RP) plant extract exhibits protective effects on cerebral ischemia. This effect is reflected in altered ischemic neuronal apoptosis and associated protein expression. OBJECTIVE: To explore the neuroprotective mechanism of RP after cerebral ischemia injury DESIGN, TIME AND SETTING: Randomized control experiment of cellular, molecular, and protein levels. The experiment was completed at Chongqing Medical University at the School of Pharmacy Laboratories and Basic Medical Institute from October 2005 to January 2006. MATERIALS: Twenty-four adult , male, Wistar rats, weighing (28 ± 20) g. RP extract, which was a product of ethanol extraction, was provided by the Laboratory of Pharmaceutical Analysis, Chongqing Medical University. RP was dissolved in distilled water to a concentration of 10 mg / mL. All rats were randomly assigned into four groups: 5 g / kg RP, 10 g / kg RP, model, and sham-surgery, with 6 rats in each group. METHODS: In the 5 and 10 g / kg RP groups, as well as the model group, the middle cerebral artery was occluded (MCAO) for 60 minutes, resulting in focal cerebral ischemia, followed by reperfusion for 24 hours. Rats in the 5 and 10 The RP treatment group received RP intragastrically (once a day) for 3 days. One hour after the last dose, rats were subjected to MCAO. The same surgical procedure was performed in the sham-surgery group, except the suture was introduced into the external carotid artery, but not advanced. Rats in the model group were subjected to MCAO. The sham-surgery and model groups received intragastrically normal saline once per day for 3 one hour after the last dose, the rats were subjected to surgery. MAIN OUTCOME MEASURES: TUNEL labeling and immunohistochemical methods were used to in vestigate changes in neuronal apoptosis and expression of the apoptosis-related proteins, Bax and Bcl-2, on the ischemic hCompared with the sham-surgery group, the number of the TUNEL-positive cells in the model group, as well as the 5 and 10 g / kg RP treatment groups, were significantly increased in the ischemic hemisphere (P <0.05). Compared with the sham-surgery group, the number of Bcl-2-positive and Bax The number of Bcl-2-positive cells increased, and the number of Bax-positive cells decreased in the model group, compared to the 5 and 10 g / kg RPs (P <0.01) treatment groups (P <0.05-0.01). CONCLUSION: RP can prevent neuronal apoptosis following cerebral ischemic-reperfusion of rats. The mechanism underlying the RP-induced neuroprotection in the cerebral ischemia injury may be related to increased Bcl-2 expression and decreased Bax expression.