背根神经节CB2受体介导的丹皮酚抗痛经机制研究

原发性痛经是指无明显盆腔器质性病变而出现月经期下腹部痉挛性疼痛的一类疾病。发病率高，已严重影响年轻女性的工作和生活质量，其发病机制主要与子宫平滑肌痉挛性收缩、子宫缺血等有关，目前治疗手段有限。前期研究发现：丹皮酚可通过CB2R阻断子宫平滑肌细胞内的L型Ca2+通道和钙内流，抑制子宫平滑肌收缩。而CB2R在体内分布广泛，除了外周系统，还大量表达于神经系统。背根神经节作为初级感觉神经元胞体所在地，同样存在CB2R 的表达，钙离子作为一种重要的第二信使，则参与了痛觉信号的形成和传播。因此推测丹皮酚抗痛经作用还可能与激活背根神经节神经中的CB2受体，阻断Ca2+参与的痛觉神经的传播和突触兴奋的形成有关。本研究旨在探讨丹皮酚对大鼠原发性痛经模型中背根神经节CB2受体、下游蛋白表达及钙通道电流的影响，阐明丹皮酚对痛经大鼠痛觉信息加工及传递的影响及机制。

Primary dysmenorrhea refers to a kind of disease without obvious organic pelvic disease and abdominal spasm pain during menstruation. The high incidence has seriously affected the work and life quality of young women. Its pathogenesis is mainly related to spasticity, uterine ischemia and so on. Previous studies showed that paeonol could block L-type Ca2+ channels and calcium influx in uterine smooth muscle cells through CB2r, and inhibit contraction of uterine smooth muscle cells. CB2r is widely distributed in the body. Besides peripheral system, it is also expressed in nervous system. The dorsal root ganglion is the site of primary sensory neurons and the expression of CB2r was exist. As an important second messenger, calcium participates in the formation and transmission of pain signals. Therefore, it is speculated that the anti dysmenorrhea effect of paeonol may be related to the activation of CB2 receptor in DRG ，block the transmission of pain nerve and the formation of synaptic excitation. The purpose of this study is to investigate the effects of Paeonol on the expression of CB2 receptor, downstream protein and calcium channel current in the dorsal root ganglia of rats with primary dysmenorrhea.