Neuroprotection of dexmedetomidine against propofol-induced neuroapoptosis partly mediated by PI3K/Akt pathway in hippocampal neurons of fetal rat

作     者：Ning ZHANG Quan-ping SU Wei-xia ZHANG Nian-jun SHI Hao ZHANG Ling-ping WANG Zhong-kai LIU Ke-zhong LI 

作者机构：Department of Anesthesiology the Second Hospital of Shandong University Department of Anesthesiology Linyi People’s Hospital The Central Laboratory Linyi Peoples’ Hospital Intensive Care Unit Linyi People’s Hospital 

出 版 物：《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 (浙江大学学报（英文版）B辑（生物医学与生物技术）)

年 卷 期：2017年第18卷第9期

页      面：789-796页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 0905[农学-畜牧学] 0906[农学-兽医学] 100217[医学-麻醉学] 10[医学] 

基　　金：supported by the Medical and Health Technology Development Program in Shandong Province(No.2015WSA13033) the National Natural Science Foundation of China(No.81301114) 

主　　题：Dexmedetomidine Propofol Neuroapoptosis PI3K/Akt 

摘      要：The aim was to investigate how the PI3K/Akt pathway is involved in the protection of dexmedetomidine against propofol. The hippocampal neurons from fetal rats were separated and cultured in a neurobasal medium. Cell viability was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay. Then neurons were pretreated with different concentrations of dexmedetomidine before 100 μmol/L propofol was added. Akt, phospho-Akt(p-Akt), Bad, phospho-Bad(p-Bad), and Bcl-x L were detected by Western blot. Also, neurons were pretreated with dexmedetomidine alone or given the inhibitor LY294002 before dexmedetomidine pretreatment, and then propofol was added for 3h. The results demonstrated that propofol decreased the cell viability and the expression of p-Akt and p-Bad proteins, increased the level of Bad, and reduced the ratio of Bcl-x L/Bad. Dexmedetomidine pretreatment could reverse these effects. The enhancement of p-Akt and p-Bad induced by dexmedetomidine was prevented by LY294002. These results showed that dexmedetomidine potently protected the developing neuron and this protection may be partly mediated by the PI3K/Akt pathway.