远志YZ-50对慢性应激抑郁模型大鼠海马Bax、Bcl-2表达的影响 |
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引用本文: | 谢婷婷,刘屏,孙艳,王东晓,陈桂芸.远志YZ-50对慢性应激抑郁模型大鼠海马Bax、Bcl-2表达的影响[J].中国药物应用与监测,2008,5(6):14-17. |
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作者姓名: | 谢婷婷 刘屏 孙艳 王东晓 陈桂芸 |
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作者单位: | 解放军总医院药品保障中心,北京,100853 |
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基金项目: | 国家自然科学基金资助项目
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摘 要: | 目的:探讨远志YZ-50对慢性应激抑郁模型大鼠海马神经元凋亡因子Bax、Bcl-2表达的影响。方法:采用健康雄性Ⅱ级Wistar大鼠慢性应激抑郁模型,通过免疫组化染色法检测模型大鼠海马区凋亡调控因子Bax、Bcl-2蛋白的表达,从分子水平探讨在给予远志YZ.50后凋亡调控因子Bax、Bcl-2在慢性应激抑郁大鼠海马组织的变化规律。本实验共设五组,分别是空白对照组、慢性应激模型组、地昔帕明组(20mg·kg^-1)、YZ-50低剂量组(2.8g生药·kg^-1)、YZ-50高剂量(5.6g生药·kg^-1)组。结果:在给予大鼠慢性应激刺激21d,造成应激抑郁模型后,通过检测表明模型组动物Bax蛋白的表达明显增加,Bcl-2蛋白表达很弱;YZ-50低、高剂量组动物Bcl-2蛋白的表达与模型组动物相比明显增加;Bax蛋白的表达与模型组动物相比均显著降低(P〈0.05)。结论:YZ-50能够提高慢性应激抑郁模型大鼠海马区CA3区Bcl-2蛋白的表达、抑制Bax蛋白的表达,调控Bcl-2/Bax比例而抑制神经细胞的凋亡,减少外界刺激对脑部神经元的损害,从而改善其抑郁状态。
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关 键 词: | 远志 抗抑郁 免疫组化 Bax Bcl-2 |
Effect of polygala tenuifolia willd YZ-50 on expression of the Bax,Bcl-2 of chronic stress depression rats |
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Authors: | XIE Ting-ting LIU Ping SUN Yan WANG Dong-xiao CHEN Gui-yun |
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Institution: | (PLA General Hospital, Beijing, 100853) |
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Abstract: | Objective: To investigate the effect of polygala tenuifolia willd YZ-50 on expression of the Bax, Bcl-2 of chronic stress depression rats. Methods: Expression of the Bax, Bcl-2 in the chronic stress depression rats' hippoeampus was detected by immunohistoehemistry methods with the healthy male Ⅱ grade wistar rats of chronic stress depression rats and the change rule of the Bax, Bcl-2 was discussed from molecular level. Experiment was allocated randomly to five groups: normal control group, model group, desipramine group (20 mg · kg^-1) and polygala tenuifolia willd YZ-50 low (2.8 g · kg^-1 dried medicinal herb) and high (5.6 g · kg^-1 dried medicinal herb) dosage groups. Results: When the chronic stress depression rats model was built successfully, results demonstrated that the expression of the Bax was increased obviously and the Bcl-2 expressed lowly in the model group; Compared with model group, the Bcl-2 showed up-regulation in each dosage of YZ-50, while the Bax decreased significantly (P 〈 0.05). Conclusion: YZ- 50 increased the expression of Bcl-2, inhibited the expression of Bax, controlled the proportion of Bcl-2/Bax to reduce the apoptosis of the neurons and decreased the outside impaired effect towards neurons which improved the depressive state. |
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Keywords: | Bax Bcl-2 |
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