摘要
目的:通过观察慢性应激抑郁模型大鼠接受电针刺激后海马神经元凋亡的情况和JNK信号转导通路的变化,探讨电针治疗抑郁症的作用机制。方法:65只SD大鼠,随机分为空白组、空白电针组、模型组、电针组、百优解组。采用慢性应激结合孤养的方式造模。电针组给予电针"百会""印堂"穴,每次20 min,每日1次,共治疗21 d;百优解组给予百优解1.8 mg/kg灌胃治疗,共21 d。采用旷场实验进行行为学评价;采用AnnexinV-FITC流式细胞凋亡检测方法检测海马神经元凋亡;采用免疫印迹技术半定量检测JNK碱性磷酸酶活化水平。结果:模型组大鼠旷场实验3 min内水平穿越格数、竖立次数均明显低于空白组(均P<0.05);海马神经元细胞凋亡率明显高于空白组(P<0.05)。3 min内旷场实验各指标电针组、百优解组均明显高于模型组(P<0.05);电针组和百优解组海马神经元细胞凋亡率均明显低于模型组(P<0.05)。各组大鼠海马组织中JNK磷酸酶活化水平,模型组高于空白组(P<0.05),电针组、百优解组均低于模型组(P<0.05)。空白电针组各指标的变化与空白组相似(P>0.05)。结论:电针可能通过有效地抑制JNK磷酸酶活化,同时抑制海马神经元凋亡而改善慢性应激抑郁大鼠的行为学症状。
Objective To observe the effect of electroacupuncture（EA） on hippocampal apoptosis and c-Jun N-terminal kinase（JNK） signal pathway in chronic stress depression rats so as to study its mechanism underlying acupuncture-induced improvement of depression.Methods Sixty-five SD rats were randomly divided into control,control＋EA,model,EA and Prozac groups,with 13 rats in each.Open-field test was used to detect the rats＇ behavior changes.The apoptotic rate of the hippocampal cells was detected by Annexin V fluorescein isothiocyanate（FITC）/ Propidium iodide（PI）（Annexin V-FITC/PI） double-staining,and the expression of hippocampal JNK protein detected by Western blot.Results After repeated stress stimulation（21 days）,the crossing numbers（1.8±0.2） and rearing times（0.5±0.1） in the model group were apparently lower than those（48.1±18.3,14.2±2.4）in the control group and those（47.2 ±15.8,13.5±2.6）in the control＋EA group（P0.05）.Compared with the model group,the crossing numbers and rearing times（40.2±10.1,10.3±2.2） during 3 min in the EA group and those（39.8±12.4,10.6±3.2） in the Prozac group were increased considerably（P0.05）.The hippocampal apoptotic rate was significantly higher in the model group（67±10） than in the control（53±13） and control＋EA groups（52±10,P0.05）.In comparison with the model group,the apoptotic rate（29±9） of the EA group and that（51±13） of the Prozac group were significantly lower（P0.05）.Compared with the control group,the phosphorylated JNK（p-JNK） level was considerably higher in the model group（P0.05）;while compared with the model group,the p-JNK level was significantly lower in the EA and Pozac groups（P0.05）.No apparent differences were found between the EA and and Prozac groups in the aforementioned indexes（P0.05）.Conclusion EA can reduce hippocampal apoptotic rate and down-regulate hippocampal p-JNK level in depression rats,which is responsible for its effect in improving depression-induced decreased movement.
出处
《针刺研究》
CAS
CSCD
北大核心
2010年第5期330-334,共5页
Acupuncture Research
基金
国家自然科学基金重点课题面上项目(90709034)
