Effect of propofol on cyclooxygenase-2 expression in hippocampal neurons in depressed rats after electroconvulsive therapy
10.3760/cma.j.issn.0254-1416.2012.02.005
- VernacularTitle:异丙酚对抑郁大鼠电休克治疗后海马神经元环氧化酶-2表达的影响
- Author:
Xiaobin LIU
;
Su MIN
;
Jie LUO
;
Chao LIU
;
Wei LI
;
Xiao LI
- Publication Type:Journal Article
- Keywords:
Propofol;
Depressive disorder;
Electroconvulsive therapy;
Cyclooxygenase 2;
Hippocampus
- From:
Chinese Journal of Anesthesiology
2012;32(2):154-157
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effect of propofol on cyclooxygenase-2 (COX-2) expression in hippocampal neurons in depressed rats after electroconvulsive therapy (ECT).MethodsFifty 2-3 months old male SD rats weighing 200-250 g were randomly divided into 5 groups (n =10 each):group control (group C) ; group depression (group D); group propofol (group P); group ECT (group E) and group propofol + ECT (group PE).Depression was induced by separation and chronic unpredictable mild stres in groups D,P,E and PE.Groups P and PE received intraperitoneal pro pofol 80 mg/kg.Groups E and PE received ECT at 5 min after IP normal saline 8 ml/kg and propofol 80 mg/kg respectively once a day for 7 consecutive days.The learning and memory function was assessed by using Morris water maze test before (baseline) and after depression was induced and ECT.The animals were then sacrificed and their brains removed for detection of COX-2 mRNA expression in hippocampus (by RT-PCR).Results In group D depression significantly prolonged evasive latency and decreased swimming time percentage in platform quadrant and up-regulated COX-2 mRNA expression as compared with group C.In group E ECT further prolonged evasive latency and up-regulated COX-2 mRNA expression in depressed rats.In group PE propofol pretreatment attenuated ECT-induced impairment of learning-memory function and increase in COX-2 mRNA expression as compared with group E.ConclusionPropofol can ameliorate the decrease in learning and memory function induced by ECT in depressed rats by inhibiting COX-2 expression in hippocampal neurons.
