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Juan Sun, Jian Wang, Luoman Hu, Jinfeng Yan Rehabilitation Department, The Affiliated Hospital of Qingdao University, Qingdao City, Shandong Province 266000, People’s Republic of ChinaCorrespondence: Juan SunRehabilitation Department, The Affiliated Hospital of Qingdao University, No. 1677 Wutaishan Road, Qingdao City, Shandong Province 266000, People’s Republic of ChinaEmail yg4170@163.comBackground/Aims: Ischemic stroke is the main cause of nerve damage and brain dysfunction, accompanied by strong brain cell apoptosis. This study aimed to investigate the effect of kaempferol-3-O-rhamnoside (K-3-rh) on cerebral ischemia-reperfusion (I/R) injury.Methods and Materials: A rat model of cerebral I/R injury was established. The effects of K-3-rh on cerebral infarction size, brain water content and neurological deficits in rats were evaluated. Apoptosis of ischemic brain cells after mouse I/R was observed by TUNEL staining and flow cytometry. Western blot and qRT-PCR were used to detect the effect of K-3-rh on the expression of apoptosis-related proteins.Results: K-3-rh can improve the neurological deficit score, reduce the infarct volume and brain water content, and inhibit cell apoptosis. In addition, K-3-rh significantly downregulated the expression of Bax and p53 and upregulated the expression of Bcl-2, and the phosphorylation level of Akt. Blockade of PI3K activity by the PI3K inhibitor wortmannin not only reversed the effects of K-3-rh on infarct volume and brain water content but also reversed the expression level of p-Akt.Conclusion: K-3-rh had obvious neuroprotective effects on brain I/R injury and neuronal apoptosis, and its mechanism may be related to activation of PI3K/Akt signaling pathway.Keywords: kaempferol-3-O-rhamnoside, PI3K; Akt, apoptosis, cerebral ischemia/reperfusion injury