Neuroprotective Effect and Mechanism of Glycosides of Cistanche on Cerebral Ischemia-Reperfusion Injury in Rats Based on PI3K-Akt Signaling Pathway
Objective To investigate the protective effects and mechanisms of glycosides of cistanche (GCs) on cerebral ischemia-reperfusion injury (CIRI) in rats by activating PI3K-Akt signaling pathway.Methods Sixty male Wistar rats were randomly divided into the sham group,the model group,the GCs group and the nimodipine group.The modified embolism method was used to construct a rat model of CIRI.The deficits in the central nervous system of rats in each group were assessed by the Zea-Longa neurological function score.The area of cerebral infarction of rats in each group was calculated by 2,3,5-triphenyltetrazolium chloride staining.The apoptosis rate was detected by terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining.The expression of apoptosis-related factors was analyzed by immunofluorescence staining.Western blot and fluorogenic quantitative PCR were used to detect the expression levels of apoptosis-related factors and molecules related to the PI3K-Akt signaling pathway in each group of rats.Results Compared with the sham group,the CIRI model rats exhibited severe neurological deficit symptoms,increased neurological function scores (P＜0.05),reduced motor function,enlarged cerebral infarction area,increased apoptotic cells,and elevated expression of pro-apoptotic factors B-cell lymphoma-2 (Bcl-2) associated X protein (Bax) and cytochrome C (CytC) (P＜0.05).The expression levels of Bcl-2,Bcl-2/Bax,phosphoinositide 3-kinase (PI3K),phospho-protein kinase B (p-Akt),and p-Akt/Akt were decreased (P＜0.05).Compared with the model group,GCs promoted the recovery of motor function,reduced the area of cerebral infarction,regulated neuronal apoptosis,inhibited the expression of Bax and CytC (P＜0.05),and promoted the expression of Bcl-2,Bcl-2/Bax,PI3K,p-Akt,and p-Akt/Akt in CIRI model rats.Conclusions GCs may exert neuroprotective effects on CIRI model rats by activating the PI3K-Akt signaling pathway and inhibiting neuronal apoptosis.
PI3K-Akt signaling pathwayCerebral ischemia reperfusionGlycosides of cistancheApoptosisNervous system
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维普
