摘要
目的:从磷脂酰肌醇(PI)信号传导通路上重要调节因子IP3的角度,探讨脑缺血后抑郁模型磷脂酰肌醇(PI)信号传导通路的变化及中药颐脑解郁方的干预作用。方法:在脑缺血后抑郁模型上,采用AlphaScreen受体竞争机制,观察脑缺血后抑郁大鼠前额叶皮层、海马IP3含量的变化及中药颐脑解郁方的干预作用。结果:脑缺血后抑郁模型大鼠皮层及海马IP3含量明显高于正常组,模型组IP3的含量明显高于治疗组。结论:脑缺血后抑郁模型大鼠脑皮层及海马IP3含量增加,中药颐脑解郁方能使之明显下调,提示脑缺血后抑郁IP3含量增加,颐脑解郁方的抗抑郁作用可能与调节受体后PI信号通路有关。
Objective： To observe the expression and change of PI on phosphatidyl inositol signal pathway in rats with post-stroke depression in view of IP3 which is nuclear transcription factor-second messenger as well as interference effect of Yi-nao-jie-yu Formula on it. Method ： Amplified Luminescent Proximity Homogeneous IP3 Assay was used in the rat model of post-stroke depression. The biotinylated IP3 analog depleted the unlabeled IP3 competitor, allowing the two AlphaScreen beads to bind via the antibody interaction. As a result, an intense AlphaScreen signal was generated. The expression of IP3 in prefrontal Cortex and hippocampus and the interference of Yi-nao-jieyu Formula were observed. Result ： The expression of IP3 in hippocampus and prefrontal cortex in the rat model of post-stroke depression in the treatment group increased more obviously than that in the normal group, and IP3 in model group was more than in the treatment group. Conclusion ： The expression of IP3 in the brain of rat model of post-stroke depression increases, while Yi-nao-jie-yu Formula can decrease the expression. It shows that the expression of IP3 increased in rat with post-stroke depression, and the anti-depression effect of Yi-nao-fie-yu Formula may be related to the function of improving IP3 expression.
出处
《山西中医》
2009年第2期39-41,共3页
Shanxi Journal of Traditional Chinese Medicine
基金
国家自然科学基金中标课题(项目批准号:30572389)
博士点课题代码:2005006014
关键词
脑缺血后抑郁
磷脂酰肌醇信号传导通路
三磷酸肌醇
颐脑解郁方
实验研究
post-stroke depression, phosphatidyl inositol signal pathway, inositol triphosphate, Yi-nao-fie-yu Formula, empirical study
