摘要
目的观察心肌梗死后抑郁大鼠行为学及前炎症因子的表达规律,揭示心肌梗死后抑郁发生的机制,为心肌梗死后抑郁的治疗提供药物作用的靶点。方法采用手术法结扎大鼠心脏冠状动脉左前降支制作大鼠心肌梗死模型,术后用前炎症细胞抑制剂己酮可可碱腹腔注射进行治疗,采用蔗糖水消耗实验,自发行为实验,强迫游泳实验观察大鼠行为学变化,并检测大鼠血清和脑中肿瘤坏死因子α和白细胞介素1β的含量变化。结果大鼠急性心肌梗死后2周,与假手术组相比,模型组大鼠的蔗糖水消耗量,及活动总路程、站立时间、活动总时间、游泳时间和挣扎时间减少,不动时间增多,炎症因子肿瘤坏死因子α和白细胞介素1β均明显增多(P<0.05,或P<0.01)。结论心肌梗死后大鼠出现活动度下降,快感缺乏,产生绝望行为以及血浆内和脑内炎症因子升高,在使用己酮可可碱后其行为活动度升高及绝望行为减缓,血浆内和脑内炎症因子下降,提示阻断炎症反应过程,可以改善大鼠心肌梗死后的抑郁状态,提示炎症反应可能是心梗后抑郁发生的可能机制。
Objective To investigate the behavior and expression pattern of pro-inflammatory cytokine in rat model of depression after acute myocardial infarction,and to provide a kind of animal models for studying the mechanism of depression after myocardial infarction. Methods The rats were given thoracotomy and left front descending coronary artery ligation to induce acute myocardial infarction model. Pro-inflammatory inhibitor pentoxifylline was administered after the operation. Sucrose water consumption test,open-field test and forced swimming test were used to evaluate the behavior changes of the rats. IL-1β and TNF-α in both serum and brain of rats were detected to evaluate the changes of inflammatory cytokines.Results Compared with the sham-operation group,the scores of horizontal movement,vertical movement,consumption of sucrose water,the swimming time,the struggling time were significantly decreased in AMI group while the immobility time and the content of inflammatory cytokines were increased(P〈0. 05,orP〈0. 01). Conclusion After myocardial infarction,the rats decrease activity,lose interests in new en-vironment,lack of pleasure,become behavioral despair,but increase the content of inflammatory cytokines. However,after injected with Pentoxifylline,the rats increase activity,decrease the behavioral despair and the content of inflammatory cytokines. All the above indicate inflammatory response could be the mechanism of depression after myocardial infarction.
出处
《环球中医药》
CAS
2015年第12期1446-1451,共6页
Global Traditional Chinese Medicine
基金
国家自然科学基金(81072713)
关键词
心肌梗死
抑郁
炎症反应
前炎症细胞因子
Myocardial infarction
Depression
Inflammatory reactions
Pro-inflammatory cytokine