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机构地区:[1]山东省中医院,济南250011 [2]山东中医药大学药学院,济南250355
出 处:《长春中医药大学学报》2015年第5期893-896,共4页Journal of Changchun University of Chinese Medicine
基 金:山东省2011-2012年度中医药科技发展计划项目(2011-75)
摘 要:目的探讨逍遥散对抑郁模型大鼠海马中神经递质(5-HT、NE、DA)的含量及海马脑源性神经营养因子(BDNF)和其受体型酪氨酸蛋白激酶B(Trk B)表达的影响,揭示逍遥散抗抑郁的机制。方法将SD雄性大鼠50只随机分为正常组,模型组,盐酸氟西汀组(3 mg/kg),逍遥散高、低剂量组(14、7 g/kg)。除正常组外,对其余各组大鼠进行56 d的孤养加慢性应激刺激,第29天起灌胃给药,连续给药28 d,给药结束后解剖大鼠取海马。采用放免法测定大鼠海马中神经递质5-HT、DA、NE的含量变化;采用免疫组化法检测海马中BDNF和Trk B阳性神经元面密度值的变化。结果与正常组相比,模型组大鼠海马中5-HT、DA、NE的含量显著下降,BDNF和Trk B阳性神经元面密度值显著减小(P<0.01),与模型组相比,逍遥散高、低剂量可以显著增加海马中5-HT、DA、NE的含量,明显提高BDNF和Trk B阳性神经元面密度值(P<0.05或P<0.01)。结论逍遥散可明显改善抑郁模型大鼠的抑郁状态,其机制与其可增加相关神经递质的含量,增强BDNF和Trk B表达有关。Objective To study the effect of Xiaoyaosan on the cotent of nurotransmitter of depression model SD Rats hippocampus,and on brain-derived neurotrophic factor and the expression of receptor Trk B of its hippocampus,to reveal the mechanism of antidepressant of Xiaoyaosan. Methods We equally assign 50 male rats into a normal,a model,a Fluoxetine( 3 mg·kg),and a high or low of Xiaoyaosan group( 14. 7 g·kg). Except the normal group,we conducted 56-day separation and chronic stress stimulation on the remaining rats. From the twenty-ninth day,we will dose the rats by ig,continuous administration for 28 days. After the end of dosing,anatomize the rats to get their hippocampus. Determinate the changes of 5-HT,DA,NE contenting in neurotransmitter of the rats hippocampus by radioimmune assay. Test the changes of BDNF and Trk B's Positive neurons surface density values by immunohistochemistry. Results Compared with the normal group,the content of 5-HT,DA,NE in hippocampus of model group rats decreased significantly,and so do BDNF and Trk B positive neurons surface density values( P〈0. 01). Compared with the model group,high or low dosage of Xiaoyaosan can be significantly increased the content of 5-HT,DA,NE in the hippocampus and BDNF and Trk B positive neurons surface density values( P〈0. 05 or P〈0. 01). Conclusion Xiaoyaosan can significantly improve the depressive state of depression model rats. Its mechanism is associated with the increasing content of related neurotransmitters and the enhancing BDNF and Trk B expression.
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