부산대학교 도서관

Introduction Cardiopulmonary bypass (CPB) is considered indispensable during heart operations, but the potential adverse effects on sensitive organs, such as the brain or the kidneys, cannot be ignored (1). In [...]
[alpha]7 nicotinic acetylcholine receptor ([alpha]7nAchR) agonist treatment may provide a promising therapeutic effect for cerebral injuries. However, it is unclear whether the activation of [alpha]7nAchR agonist may reduce cerebral injuries induced by cardiopulmonary bypass (CPB). A total of 96 male Sprague-Dawley rats were randomly divided into four groups (n=24/group): i) Sham operation group; ii) CPB group; iii) CPB + [alpha]7nAchR agonist group; and iv) CPB + [alpha]7nAchR agonist + [alpha]7nAchR antagonist group. Following treatment, 24 rats from each group were sacrificed and the serum and hippocampal tissues were collected. The serum expression levels of S100[beta], interleukin 6 and tumor necrosis factor [alpha] were evaluated by ELISA, hippocampal tissues were analyzed by histopathological examination using hematoxylin & eosin and terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling (TUNEL) staining and Caspase 3 expression in the hippocampal tissues was evaluated by immunohistochemistry. In addition, Caspase 3, Akt and glycogen synthase kinase 3[beta] (GSK3[beta]), as well as phosphorylated (p)-Akt and (p)-GSK3[beta] were examined by western blot assay. The present study demonstrated that [alpha]7nAchR agonist treatment was able to alleviate pathological damage and inhibit hippocampal cell apoptosis and inflammatory response. [alpha]7nAchR agonist treatment also increased the expression levels of p-Akt and p-GSK3[beta], which indicated an upregulation in Akt/GSK3[beta] signaling. These data suggested that [alpha]7nAchR agonist may provide a promising new therapeutic approach for cerebral injury caused by CPB. Key words: [alpha]7 nicotinic acetylcholine receptor, cardiopulmonary bypass, apoptosis, Caspase 3, Akt/glycogen synthase kinase 3[beta] pathway