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鞘内注射氨甲环酸对脊髓胶质细胞反应性的调节不足以抑制神经挤压诱导的机械性异常性疼痛。

Modulation of spinal glial reactivity by intrathecal PPF is not sufficient to inhibit mechanical allodynia induced by nerve crush.

作者信息

Gallo Alessandro, Dimiziani Andrea, Damblon Jonathan, Michot Benoît, Des Rieux Anne, De Kock Marc, Hermans Emmanuel, Deumens Ronald

机构信息

Institute of Neuroscience, Université catholique de Louvain, Avenue Hippocrate B1.54.10, 1200 Brussels, Belgium.

Louvain Drug Research Institute, Pharmaceutics and Drug Delivery Unit, Avenue E. Mounier 73, 1200 Brussels, Belgium.

出版信息

Neurosci Res. 2015 Jun;95:78-82. doi: 10.1016/j.neures.2015.02.004. Epub 2015 Feb 16.

DOI:10.1016/j.neures.2015.02.004
PMID:25697394
Abstract

Spinal glial reactivity has been strongly implicated in pain that follows peripheral nerve injury. Among the many therapeutic agents that have been tested for anti-allodynia through immune modulation is the atypical methylxanthine propentofylline. While propentofylline shows a potent anti-allodynia effect after nerve transection injury, we here demonstrate that, when propentofylline is used intrathecally at the effective immune-modulatory dose, allodynia after rat nerve crush injury is completely preserved. Microglial/macrophage Iba-1 and astrocytic GFAP expression, increased in the dorsal horn of nerve crushed animals, was, however, effectively attenuated by propentofylline. Effective modulation of spinal glial reactivity is, thus, no assurance for anti-allodynia.

摘要

脊髓胶质细胞反应性与周围神经损伤后的疼痛密切相关。在众多通过免疫调节测试抗异常性疼痛的治疗药物中,非典型甲基黄嘌呤丙戊茶碱是其中之一。虽然丙戊茶碱在神经横断损伤后显示出强大的抗异常性疼痛作用,但我们在此证明,当以有效的免疫调节剂量鞘内注射丙戊茶碱时,大鼠神经挤压损伤后的异常性疼痛完全保留。然而,丙戊茶碱有效减弱了神经挤压动物背角中微胶质细胞/巨噬细胞Iba - 1和星形胶质细胞GFAP的表达增加。因此,有效调节脊髓胶质细胞反应性并不能保证抗异常性疼痛。

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