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目的:观察帕罗西汀对心理应激大鼠下丘脑c fos表达的影响,以揭示帕罗西汀治疗心理应激引起焦虑的分子作用机制。方法:建立大鼠心理应激模型,观察抗焦虑药物帕罗西汀用药组大鼠血浆皮质醇和下丘脑c fos的表达。结果:与正常对照组比较,各应激组大鼠血浆皮质醇含量明显升高,下丘脑室旁核c fos表达显著增加,而帕罗西汀单次、连续给药能减少应激大鼠血浆皮质醇含量和下丘脑室旁核c fos表达。结论:帕罗西汀通过抑制c fos基因表达,下调下丘脑垂体肾上腺轴(HPA轴)水平,从而发挥中枢应激调节作用。
OBJECTIVE: To observe the effect of paroxetine on the c fos expression in the hypothalamus of rats under psychological stress to reveal the molecular mechanism of paroxetine in the treatment of psychological stress-induced anxiety. Methods: The rat model of psychological stress was established to observe the expression of cortisol and c fos in hypothalamus of paroxetine-treated rats. Results: Compared with the normal control group, the plasma cortisol levels were significantly increased in each stress group and the c fos expression in the paraventricular nucleus of hypothalamus was significantly increased. However, single and continuous administration of paroxetine could reduce the plasma cortex Alcohol content and c fos expression in hypothalamic paraventricular nucleus. CONCLUSION: Paroxetine exerts the central stress regulation by inhibiting c fos gene expression and down-regulating the level of hypothalamic-pituitary-adrenal axis (HPA axis).