The elucidation of the reconstruction mechanism of the nucleus tractus spinalis sensory nerve in region of face cancer pain and the neuropathic pain

在这项研究中，我们阐明了脊神经-胶质细胞相互作用对大鼠眶下区癌性疼痛和/或神经病理性疼痛的影响，并对其进行研究，以获得神经营养因子治疗是否有效的潜在发现。首先通过大鼠眶下区注射弗氏佐剂或Walker 256 B制作炎症性疼痛和癌性疼痛大鼠模型，并对炎性疼痛大鼠和癌性疼痛大鼠分别给予消炎痛消炎痛和癌痛大鼠消炎痛，以确定两种疼痛的差异。此外，我们还确定了c-fos基因在神经病理性疼痛和癌性疼痛大鼠的分叶切除早期的表现。神经病理性疼痛大鼠和癌性疼痛大鼠分别给予COX-II抑制剂、p38MAPK抑制剂和小胶质细胞失活剂后，疼痛行为明显受到抑制。在神经病理性疼痛中，脊髓谷氨酸神经系统的激活在…早期发生P38-MAPK的发生、激活和激活依次发生，脊髓神经系统的突触传递明显改变，周围作为炎症电荷细胞的小胶质细胞将其激活，并与COX-II结合，激活和分离脑源性神经营养因子p38-MAPK，并在神经病理性疼痛中发展。对三叉神经节切断后的GFAP、IBA1进行免疫组织化学染色，分别检测小胶质细胞和星形胶质细胞在神经病理性疼痛和癌性疼痛大鼠中的贡献。无论是神经性疼痛还是癌性疼痛，小胶质细胞的激活均早于疼痛发作，而星形胶质细胞激活的时间较晚。此外，当皮下注射小胶质细胞灭活剂给癌症疼痛大鼠时，发现癌症疼痛显著减少。这一结果发现，脊髓-小胶质细胞的相互作用参与了神经病理性疼痛和癌性疼痛的疼痛机制。较少

In this study, we elucidated effect of the spinal nerve-glia interaction on cancer pain and/or neuropathic pain of the rat regio infraorbitalis and studied it for the purpose of obtaining an underlying finding whether or not the treatment by the neurotrophy factor was effective. At first we made the inflammatory pain and cancer pain rat model that injected Freund's adjuvant or Walker 256 B into the rat regio infraorbitalis and gave antiphlogistic indomethacin to an inflammatory pain rat and a cancer pain rat to determine difference in both pain. Furthermore, we determined manifestation by the early period of onset of the c-fos gene in the merotomy of the neuropathic pain and the cancer pain rat. The pain behavior significantly inhibited it with each drug when COX-II inhibitor, p38MAPK inhibitor, microglial inactivator were given to the neuropathic pain and the cancer pain rat, respectively. In the neuropathic pain, activation of the spinal cord glutamate nervous system occurs early in … More the onset, and activation of p38-MAPK occurs successively, Synaptic transmission of the spinal nerre system was modified remarkably, and the microglia which was inflammation charge cells nearby activated it, and what it integrated it to be accompanied with COX-II, activation and BDNF (brain-derived neurotrophic factor) isolation of p38-MAPK, and developed in neuropathic pain became clear. We performed immunostaining of the trigeminal ganglion merotomy in GFAP, Iba1 to examine the microglia and astrocytic in neuropathic pain and the cancer pain rat contribution, respectively. Microglial activation was found early in the pain onset in both of the examination of the neuropathic pain and the cancer pain, and astrocytic activation was found late. Also, a significant decrease of cancer pain was found when subcutaneous injection of the microglial inactivator to a cancer pain rat was provided. By this result, It was found that spinal cord - microglial interaction was involved in both pain mechanisms of neuropathic pain and cancer pain. Less