帕罗西汀通过抑制大鼠偏头痛模型中的 p38 磷酸化产生镇痛作用。

Department of Neurology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, Guangdong Province, China.

Department of Neurology, First Affiliated Hospital of Jinan University, Guangzhou 510630, Guangdong Province, China.

Neural Regen Res. 2012 May 5;7(13):1006-12. doi: 10.3969/j.issn.1673-5374.2012.13.007.

In this study, a model of migraine was established by electrical stimulation of the superior sagittal sinus in rats. These rats were then treated orally with paroxetine at doses of 2.5, 5, or 10 mg/kg per day for 14 days. Following treatment, mechanical withdrawal thresholds were significantly higher, extracellular concentrations of 5-hydroxytryptamine in the periaqueductal grey matter and nucleus reticularis gigantocellularis were higher, and the expression of phosphorylated p38 in the trigeminal nucleus caudalis was lower. Our experimental findings suggest that paroxetine has analgesic effects in a rat migraine model, which are mediated by inhibition of p38 phosphorylation.

在这项研究中，通过对大鼠上矢状窦进行电刺激建立了偏头痛模型。然后，这些大鼠每天口服给予帕罗西汀 2.5、5 或 10mg/kg，连续 14 天。治疗后，机械撤药阈值显著升高，导水管周围灰质和巨细胞网状核的 5-羟色胺浓度升高，三叉神经尾核磷酸化 p38 的表达降低。我们的实验结果表明，帕罗西汀对大鼠偏头痛模型具有镇痛作用，其作用机制可能与抑制 p38 磷酸化有关。