重组BDNF与电针对神经病理痛的镇痛机制比较研究

Neuropathic pain is very difficult to cure clinically so that it is important to explore its mechanism and to search for a safe, effictive and constant treatment. After nerve injury, it can cause the unbalance between excitation and inhibition system in central nervous system that is the main etiological factor of neuropathic pain. The   criticality for treating neuropathic pain lies in recovery of injuryed nerve and regulation of central sensitization. BDNF(brain derived neurotrophic factors) can promote recovery and actification of injured nerve and participate in formation of neuropathic pain. It is effective to cure neuropathic pain by electroacupuncture, but its machanism is unknown. In our early research, we succeed in induction of lentivirus-transported BDNF gene for injuryed nerve cell to express BDNF gene stably and develope neural plerosis. In the study, we will transport Lentiviral Vector into BDNF to construct neuropathic pain model which we will interfere in by electroacupuncure. By observating dynamic development of some protains such as BDNF，TrkB（tyrosine kinase receptor B），GABAA（γ-aminobutyric acid A），KCC2（K-Cl co-transporter 2）and PKC（protein kinase C） as well as pain behavior change, we investigate whether electroacupuncture can inhibit possible induction of lentivirus-transported BDNF for neuropathic pain, while reserving neural plerosis.Through the antagonistic test of KCC2 and PKC，we further elucidate the possible machanism for electroanalgesia，it will hew out new domain for   neuropathic pain treatment and provide scientific theory.

神经病理痛是临床常见的顽疾之一，探索神经病理痛的发生机制及寻找一种安全、有效、持久的治疗方法具有十分重要意义。神经受损后，中枢系统内兴奋与抑制系统之间的失衡是造成顽固性疼痛的主要原因。治疗神经病理痛的关键在于损伤神经的修复与中枢敏化调节。BDNF既有促进神经修复及再生作用，又参与神经病理痛的形成。电针治疗神经病理痛疗效确切，但其机制尚未完全阐明。我们在前期研究中成功将慢病毒介导的BDNF基因导入受损神经细胞中，稳定表达BDNF，发挥修复作用。本研究拟通过慢病毒转载BDNF基因及电针干预转载后的神经病理痛模型，观察脊髓背角BDNF、TrkB、GABAA、KCC2、PKC的动态演变、疼痛行为及神经组织学改变，探讨电针能否抑制转载的BDNF诱发的的病理痛而保留其修复作用；通过KCC2、PKC拮抗试验进一步阐明电针镇痛的可能机制。为临床治疗顽固性神经痛提供科学的理论依据。