带状疱疹神经痛是神经病理性疼痛，患者十分痛苦，而甲钴胺有明显治疗效果，探究其治痛机制有重要意义。对水疱液检测发现治疗后局部TNF-1α减少，而EPO升高。皮下神经丛中schwann细胞（SCs）可分泌EPO。对大鼠SCs研究发现，VZV刺激下TNF-α、HIF-1α和EPO都有一过性上调。甲钴胺干预可下调TNF-α，上调HIF-1α和EPO。我们推测，VZV激活的SCs可产生神经保护分子PrPC和EPO，甲钴胺通过调节SCs的PrPC，稳定HIF-1α，促进EPO的分泌。为验证此假说，选用人SCs，分步构建PrPC，PHD2或CCS基因沉默SCs模型，与VZV共培养，同时制备组织和动物模型，采集患者皮肤组织；采用分子生物学手段，从分子，细胞到组织多层面探究SCs在VZV刺激下PrPC和EPO的表达变化，甲钴胺对HIF-1α/EPO的调节及机制。为揭示钴胺素治疗带状疱疹神经痛的机制打下基础。

Herpes zoster associated neuralgia is typical of neuropathic pain, patients is very painful. Methylcobalamin has obvious analgesic effect on it, to have the important meaning to explore the mechanism of treatment of pain. For patients with blister fluid detected local TNF-1 decreased obviously after the treatment, while EPO increased significantly. Subcutaneous plexus of Schwann cells (SCs) exist, the SCs is activated to produce PrPC and EPO has neuroprotective effect. We found that the use of VZV infected rats SCs, SCs TNF- alpha and EPO all had high expression, Mecobalamine can down regulate TNF- alpha, the up-regulated expression of HIF-1 alpha and EPO. We speculate that, Mecobalamin is regulated by SCs PrPC, the stability of HIF-1 alpha, promoting the secretion of EPO. To test this hypothesis, the selection of primary cultured human SCs, step by step construction of PrPC, PHD2 or CCS gene silencing SCs model, were co cultured with VZV cells, and tissue and animal models were prepared, from the molecular to explore multi level SCs in VZV stimulated the expression and mechanism of PrPC and EPO, regulating effect of mecobalamin on HIF-1 alpha /EPO and molecular mechanism, at the same time acquisition of skin tissue is verified. To lay the foundation for revealing the mechanism of cobalamin treatment of herpes zoster neuralgia.