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作 者:王杰琼[1] 许莉莉[1] 张丽娜[2] 薛玲[1]
机构地区:[1]山东中医药大学中医药经典理论教育部重点实验室,济南250355 [2]威海市立医院,山东威海264200
出 处:《中国实验方剂学杂志》2015年第13期105-108,共4页Chinese Journal of Experimental Traditional Medical Formulae
基 金:国家自然科学基金面上项目(81173162)
摘 要:目的:通过观察经前期综合征(PMS)肝气郁证模型大鼠下丘脑中μ-阿片受体(MOR)的蛋白表达,探讨舒郁胶囊治疗PMS肝气郁证的机制。方法:Wistar大鼠56只,随机分为正常组、模型组、舒郁胶囊组(0.408 g·kg-1)和纳洛酮组(0.4mg·kg-1),每组14只,旷场实验和阴道涂片筛选动情周期规律非接受期大鼠进入实验,除正常组,其余各组采用慢性束缚应激法复制PMS肝气郁证模型,旷场实验对模型进行行为学评价,各组大鼠下丘脑采用免疫荧光化学技术(IF)和Western blot分别观察MOR分布及蛋白表达变化。结果:宏观行为学表明,与正常组比较,模型组大鼠旷场总分显著降低(P<0.01);免疫荧光结果显示,与正常组比较,模型组大鼠下丘脑细胞分布排列杂乱且增多,与模型组比较,舒郁胶囊、纳洛酮给药组均得到显著改善;蛋白免疫印迹结果显示,与正常组比较,模型组下丘脑中MOR表达水平显著升高(P<0.01),与模型组比较,舒郁胶囊、纳洛酮给药组MOR表达水平均显著下降(P<0.01)。结论:舒郁胶囊可通过对下丘脑中MOR的拮抗作用而改善PMS肝气郁证的症状,另外,下丘脑中MOR上调可能是PMS肝气郁证的发病机制之一。Objective: To observe the effect of Shuyu capsule on μ-opioid receptors( MOR) expression in the hypothalamus of premenstrual syndrome( PMS) with liver-qi stagnation model rats,and to investigate its possible mechanism. Method: Rats were selected by using an open field test and vaginal smear in this experiment. The selected rats were divided into 4 groups: the normal group,the model group,the Shuyu capsule group( 0. 408 g·kg- 1) and the naloxone group( 0. 4 mg·kg- 1). The PMS with liver-qi stagnation model in rats was prepared by a chronic bondage stress method. The distribution and protein level of MOR in hypothalamus of rats were observed by immunofluorescence chemical technology and Western blot. Result: Compared with the normal group,the scores of open field test decreased,the distribution of messy-arranged MOR in hypothalamus increased,MOR protein expression increased in the model group( P〈0. 01). Compared with the model group,the scores of open field test increased,the distribution of messy-arranged MOR in hypothalamus decreased,MOR protein expression decreased in the Shuyu capsule and naloxone groups( P〈0. 01). Conclusion: Shuyu capsule could improve the symptoms of PMS with liver-qi depression syndrome,which may be achieved by regulating the MOR in the hypothalamus. In addition,the up-regulation of MOR in the central nervous system may be one of the pathophysiologic mechanisms.
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