¹Department of Neurology, Nanyang First People’s Hospital, Nanyang 473000, Henan Province, P.R. CHINA
²Department of Neurology, Taikang Tongji (Wuhan) Hospital, Wuhan 430050, Hubei Province, P.R. CHINA
³Department of Anesthesiology, The Hospital Affiliated to Medical School of Yangzhou University (Taizhou People’s Hospital), Taizhou 225300, Jiangsu Province, P.R. CHINA DOI : 10.9775/kvfd.2022.28345 We aimed to study the protective effects of 3-n-butylphthalide (NBP) on cerebral infarction induced by local ischemic injury and regulation mechanism of the PI3K/Akt/GSK-3β signaling pathway. One hundred male Wistar rats aged 12-15 weeks were randomly divided into 5 groups (n=20). The middle cerebral artery occlusion (MCAO) model was established. NBP, P13K specific inhibitor LY294002 and NBP plus LY294002 groups were intraperitoneally administered on the first day after modeling, once a day for 7 days. Sham operation (Sham) and model groups were intraperitoneally given equal amounts of normal saline. Neuronal damage was detected by Nissl staining. Intact neurons were counted under light microscope. The protein expressions of Akt, P-Akt, GSK-3β and P-GSK-3β were detected by Western blotting. The mNS score of NBP group decreased significantly compared with that of model group (P<0.05). Compared with model group, the cerebral infarction volume of NBP group significantly reduced (P<0.05). Compared with model group, the number of intact neurons in NBP group significantly increased (P<0.05). Compared with model group, the phosphorylation levels of Akt and GSK-3β in NBP group significantly increased (P<0.05). By activating the PI3K/Akt/GSK-3β signaling pathway, NBP relieves neurological function damage and protects against cerebral infarction induced by local ischemic injury. Keywords : Butylphthalide, PI3K, Akt, GSK-3β, Apoptosis