The Effect of Angelica sinensis Polysaccharide on Neuronal Apoptosis in Cerebral Ischemia-Reperfusion Injury via PI3K/AKT Pathway

In the present study, the protective effects and mechanism of Angelica sinensis polysaccharide (ASP) were investigated in rats with cerebral ischemia-reperfusion injury (CIRI). Rats were randomly divided into sham group, CIRI group, ASP treatment group, and ASP and LY294002 treatment group. H&E...

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Bibliographic Details
Main Authors: Haibo Xu, Jing Chen, Wenbing Liu, Hui Li, Zhenghong Yu, Chao Zeng
Format: Article
Language:English
Published: Hindawi Limited 2021-01-01
Series:International Journal of Polymer Science
Online Access:http://dx.doi.org/10.1155/2021/7829341
Description
Summary:In the present study, the protective effects and mechanism of Angelica sinensis polysaccharide (ASP) were investigated in rats with cerebral ischemia-reperfusion injury (CIRI). Rats were randomly divided into sham group, CIRI group, ASP treatment group, and ASP and LY294002 treatment group. H&E results confirmed the successful induction of CIRI in Sprague-Dawley rats. Compared with the sham group, the neurological function score, percentage of myocardial infarction area, neuronal apoptosis, oxidative stress, and inflammation in the CIRI group were significantly increased. Compared with the CIRI group, the ASP group’s neurological function score, percentage of myocardial infarction area, neuronal apoptosis, oxidative stress, and inflammation were significantly reduced. However, compared with the ASP group, LY294002 inhibited the effect of ASP in CIRI rats. CIRI downregulated the PI3K/AKT pathway and upregulated the apoptosis level. And ASP activated the PI3K/AKT pathway and Bcl-2 protein expression, while it inhibited caspase-3 and Bax expression. LY294002 could significantly inhibit the protective effect of ASP on nerve injury and the expression and phosphorylation of PI3K and Akt protein in CIRI rats. ASP could effectively improve nerve function and nerve cell apoptosis of CIRI rats by activating the PI3K/AKT signaling pathway.
ISSN:1687-9430