Neuropsychiatric Disease and Treatment (May 2020)
K-3-Rh Protects Against Cerebral Ischemia/Reperfusion Injury by Anti-Apoptotic Effect Through PI3K-Akt Signaling Pathway in Rat
Abstract
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 [email protected]/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
