基于交感-感觉偶联研究电针敏化穴缓解躯体牵涉痛效应机制

"Acupoint sensitization" represents the acupoints change from "silent" state to "sensitized" state under the pathological condition of the body, which is characterized by pathological changes and abnormal sensory conduction in the local skin of the sensitized acupoints. When visceral lesions such as chronic colitis cause sensitization of acupoints, often accompanied by somatic referred pain closely related to sympathetic-sensory coupling and neurogenic inflammation. Electroacupuncture (EA) at sensitized acupoints could reduce the release of pain related and sensitization related substances to further relieve the referred pain and promote the recovery of visceral disease. However, the potential molecular mechanisms in the dermal and the dorsal root ganglion required further investigations. Based on the previous works of our research group, We hypothesized that EA at sensitized acupoints on the body surface could alleviate visceral lesions as well as referred pain by inhibiting the neurogenic inflammation of the skin induced by sympathetic-sensory coupling in the dermal and the dorsal root ganglia. In this research, chronic colitis model will be established and the key technologies such as molecular biology, bioinformatics and genomics will be employed to determine the distribution of sensitized acupoints; Then the expression of inflammatory and pain-related substances in the skin of sensitized acupoints will be detected before and after the EA treatment, as well as the expression of specific molecular related to sympathetic-sensory coupling both in the dorsal root ganglia and the skin of sensitized acupoints. At last, the interactive mechanism between sympathetic-sensory coupling and neurogenic inflammation will be explored. This study will reveal the effect mechanism of EA at sensitized acupoints on visceral lesions and referred pain from the molecular, organ and overall levels, and thus providing basis for clinical application of sensitized acupoints.

“穴位敏化”指机体病理情况下穴位由“沉寂”态转“敏化”态的表现，体现为敏化穴局部出现病理改变及感觉异常。内脏病变如慢性结肠炎引起穴位敏化时，常伴随与交感-感觉偶联和神经源性炎性反应有关的躯体牵涉痛。电针敏化穴可减少致痛致敏物质释放并缓解牵涉痛、促进病变恢复，但其在皮肤-背根神经节相关分子机制有待进一步研究。基于课题组前期基础提出假说：电针敏化穴通过抑制皮肤-背根神经节中交感-感觉偶联所诱发体表神经源性炎性反应，缓解内脏病变及躯体牵涉痛。本研究制备慢性结肠炎模型，采用分子生物学、生物信息学、基因组学等技术，首先确定敏化穴分布和优效性；其次检测电针敏化穴前后穴区皮肤组织致炎致痛物质的表达，及皮肤-背根神经节内交感-感觉偶联相关分子的表达；最后探索交感-感觉偶联和神经源性炎性反应的交互作用。从分子、器官、系统多水平揭示电针敏化穴缓解内脏病变及躯体牵涉痛的效应机制，为敏化穴的临床应用提供实验依据。