摘要
目的:探讨经前三剂止痛方(JQF)活性部位治疗原发性痛经(primary dysmenorrheal,PD)的作用机制。方法:建立大鼠痛经模型,采用酶免法对照观察了痛经大鼠子宫前列腺素含量(PGF2α、PGE2)的变化、逆转录聚合酶链反应(RT-PCR)法检测OTR、ER-α的变化。结果:与模型组比较,JQF-A-N-30的PGF2α含量显著下降(P<0.01),JQF-A-E的PGF2α含量亦下降(P<0.05),JQF-A-N-30、JQF-A-E的PGE2含量均上升(P<0.05),PGF2α/PGE2减小(P<0.01);JQF-A-N-30、JQF-A-E的OTR、ER-α基因表达较模型组均降低(P<0.05)。结论:JQF的活性部位可以使子宫平滑肌的收缩得到抑制,从而使子宫平滑肌的紧张度降低,并能够有效的降低雌鼠痛经模型子宫组织中PGF2α的水平;通过JQF活性部位的干预,可减轻雌激素和缩宫素的刺激,从而使子宫OTR低表达,减少子宫对OT的敏感性,缓解痛经。
Objective :To investigate the mechanism of the active site of Jingqian Sanji Zhitong Formula (JQF) in trea- ting primary dysmenorrhea (PD). Methods : Dysmenorrhea model rats were established and the contents of prostaglandin ( PGF2α, PGE2 ) in uterus were observed by enzyme - immunoassay method. The expressions of OTR and ER - α were assayed by reverse transcriptase polymerase chain reaction (RT -PCR). Results:Contrasted with model group,the contentsof PGF2α in JQF - A - N - 30 group were markedly descended ( P 〈 0. 01 ). The contents of PGF2α in JQF - A - E group were also descended (P 〈0.05) while the contents of PGE2 in JQF - A - N -30 and JQF - A - E were ascend (P 〈0. 05). The ratio of PGF2a/PGE2 were also descended (P 〈 0.01 ). Compared with the model group, the expressions of OTR and ER - α genes were descended (P 〈 0. 05 ). Conclusion : The active site of JQF can effectively regulate PG expression in dysmenorrhea model rats so as to inhibit the contraction of smooth muscle of uterus and reduce the density, which may be one of the mechanisms of JQF in treating primary dysmenorrhea. It also can reduce the stimulation of ER -α and OTR by the intervention of the active site of JQF in order to lower the expression of OTR and reduce the sensibility of uterus on OTR,finally,release the dysmenorrhea.
出处
《中华中医药学刊》
CAS
2014年第11期2717-2719,共3页
Chinese Archives of Traditional Chinese Medicine
基金
天津市应用基础与前沿技术研究计划项目(13JCYBJC23900)
天津市普通高等学校本科教学质量与教学改革项目(B07-1008)
关键词
缓解痛经
大鼠痛经模型
机制研究
primary dysmenorrhea
dysmenorrhea rats model
mechanism