犬周围神经损伤后环氧合酶的表达

Shigeru Kobayashi, Yoshihiko Suzuki, S. Yamada, N. Al-khudairi, A. Meir
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引用次数: 0

摘要

为了探讨神经源性疼痛的机制,本研究采用犬正中神经压迫模型。神经被夹紧了三周。免疫组化采用亲和素-生物素-过氧化物酶复合物法,观察压迫后T细胞(CD45)和巨噬细胞(Mac-1)的变化。用抗环氧化酶(COX)-1和COX - 2抗体检测神经受压引起的这些介质的定位和变化。在对照动物中,检测到驻留T细胞,但未检测到巨噬细胞。COX-2在雪旺细胞和血管内皮细胞中呈阳性,COX-1在血管内皮细胞中检测到。神经受压后,脱髓鞘神经纤维中出现大量T细胞和巨噬细胞。巨噬细胞COX-2阳性。COX-2可能深度参与机械性压迫引起的神经炎,这种介质似乎在神经性疼痛的表现中很重要。
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Cyclooxygenase Expression in Canines Following Peripheral Nerve Injury
In order to investigate the mechanism of neurogenic pain, this study used a median nerve compression model in dogs. The nerve was compressed with a clip for three weeks. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against cyclooxygenase (COX)-1 and 2 were used to examine the localization and changes of these mediators caused by nerve compression. In control animals, resident T cells were detected, but there were no macrophages. COX-2 was positive in the Schwann cells and vascular endothelial cells, while COX-1 was detected in the vascular endothelial cells. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for COX-2. COX-2 may be deeply involved in neuritis arising from mechanical compression, and this mediator seems to be important in the manifestation of neurogenic pain.
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