Role of cPKCγ/GAP-43 signaling pathway in ketamine-induced apoptosis in hippocampal neurons of developing rats:an in vitro experiment
10.3760/cma.j.issn.0254-1416.2017.03.011
- VernacularTitle:cPKCγ/GAP-43信号通路在氯胺酮致发育期大鼠海马神经元凋亡中的作用:离体实验
- Author:
Pei ZHANG
;
Zimiao HAO
;
Sufang JIANG
;
Xuze LI
;
Lijun BO
;
Rongtian KANG
;
Zhenming DONG
;
Lining HUANG
- Keywords:
Ketamine;
Protein kinase C;
GAP-43 protein;
Child development;
Apoptosis;
Neurons
- From:
Chinese Journal of Anesthesiology
2017;37(3):296-299
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the role of conventional protein kinase Cγ (cPKCγ)/growthassociated protein-43 (GAP-43) signaling pathway in ketamine-induced apoptosis in hippocampal neurons of developing rats in an in vitro experiment.Methods Primarily cultured hippocampal neurons were seeded in culture plates at a density of 1×10.6 cells/ml and divided into 2 groups (n=10 each) using a random number table:control group (C group) and ketamine group (K group).Group C received no treatment.Ketamine was added with the final concentration of 300 μmol/L in group K.At 12 h of culture or incubation,the apoptosis in hippocampal neurons was detected by flow cytometry.The apoptotic rate was calculated.The expression of cPKCγ,GAP-43 and phosphorylated GAP-43 in hippocampal neurons was measured by Western blot.Results Compared with group C,the apoptotic rates of hippocampal neurons were significantly increased,and the expression of cPKCγ,GAP-43 and phosphorylated GAP-43 was down-regulated in group K (P<0.01).Conclusion The mechanism by which ketamine induces apoptosis in hippocampal neurons of developing rats may be related to inhibition of cPKCγ/GAP-43 signaling pathway activation in an in vitro experiment.
