OBJECTIVE：To st udy preventive effect and mec hanism of ginsenoside Rg 1 on focal cerebral ischemia-reperfusion injury（CIRI）model rats. METHODS ：Totally 78 SD rats were randomly divided into sham operation group ，model group ， butylphthalide control group （positive control ，10 mL/kg），ginsenoside Rg 1 low-dose，medium-dose and high-dose groups （10， 20，40 mg/kg），with 13 rats in each group. Administration groups were give relevant medicine intraperitoneally ，sham operation group and model group were given constant volume of normal saline intraperitoneally ，once a day ，for consecutive 7 d. After medication，except for the sham operation group ，focal CIRI model was induced by middle cerebral artery occlusion （MCAO） method in other groups. After modeling ，neurological deficit scoring was performed according to the modified neurological difict scoring standard ； TTC staining was used to detected the percentage of cerebral infarction of rats ；the cerebral water content was measured by dry/wet weight method ；serum contents of IL- 1β and IL-6 were detected by ELISA ；the protein expressions of p-p 38 MAPK and p-NF-κB p65 in cerebral tissue were determined by immunohistochemistry and Western blotting assay. RESULTS ： Compared with sham operation ，neurological deficits score ，percentage of cerebral infarction and cerebral water content ，serum contents of IL- 1β and IL-6，positive expression numbers of cells and protein expressions of p-p 38 MAPK and p-NF-κB p65 in cerebral tissue were increased significantly in model group （P＜0.05 or P＜0.01）. Compared with model group ，above index levels of administration groups were all decreased significantly （P＜0.05 or P＜0.01），and the effect of ginsenoside Rg 1 had a dose-dependent trend ；there was no significant difference of all above indexes between ginsenoside Rg 1 middle-dose，high-dose groups and butylphthalide control group （P＞0.05）. CONCLUSIONS ：Ginsenoside Rg 1 has a certain preventive effect on focal CIRI model rats ，the mechanism of which may be associated with down-regulating the protein expression of p-p 38 MAPK and p-NF-κB p65，inhibiting the release of inflammatory factors such as IL- 1β and IL-6.