Mechanism of gastrodin in cell apoptosis in rat hippocampus tissue induced by desflurane

天麻素在地氟烷致大鼠海马组织细胞凋亡中的作用机制

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作者:Luping Wang, Hushan Wang, Zongsheng Duan, Jian Zhang, Wenwen Zhang

Abstract

This study investigated the protective effect ofgastrodin on cell apoptosis in rats hippocampus tissues induced by desflurane to explore its mechanism. A total of 36 rats were randomly divided into three groups: Blank control group (C group, n=12), desflurane anesthesia group (DF group, n=12) and gastrodin treatment group (GT group, n=12). Rats in DF group were treated with anesthesia using desflurane. Rats in GT group were treated with gavage using gastrodin and the same treatment as DF group. After the experiment, novel object recognition test and water maze test were performed. The hippocampus tissues were taken from the rat after the behavioral experiment; then the number of apoptotic cells was detected using the terminal deoxynucleotidyltransferase-mediated dUTP nick end labelling (TUNEL) kit, and the mRNA and protein expression levels of p38 and interleukin-1 (IL-1) were detected via semi-quantitative polymerase chain reaction (PCR) and western blot analysis. After the desflurane anesthesia, novel object recognition showed that compared with that in DF group, the exploration capacity of novel objects in GT group was increased (P<0.01). The water maze test showed that the escape latencies in DF group, T1 in GT group was significantly shortened, but T2 was significantly prolonged (P<0.01). TUNEL assay showed that the number of apoptotic cells in hippocampus tissues in GT group was significantly fewer than that in group DF (P<0.01). Semi-quantitative PCR and western blot analysis showed that the expression levels of p38 and IL-1β in GT group were lower than those in DF group (P<0.01). The results show that gastrodin has a protective effect on the apoptosis of hippocampus cells of rats induced by desflurane. Its protection mechanism may be realized through decreasing the increased p38 and IL-1β expression levels induced by desflurane, thus blocking the p38 mitogen-activated protein kinase (p38 MAPK) pathway.

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