Neutralizing antibodies to interleukin 1-receptor reduce pain associated behavior in mice with experimental neuropathy
Neutralizing antibodies to interleukin 1-receptor reduce pain associated behavior in mice with experimental neuropathy
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白细胞介素 1 受体中和抗体可减少实验性神经病小鼠的疼痛相关行为
DOI：
10.1016/s0304-3940(99)00450-4
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发表时间：
1999
影响因子：
2.5
通讯作者：
K. Toyka
中科院分区：
文献类型：
--
作者：
C. Sommer;Sönke Petrausch;T. Lindenlaub;K. Toyka
我们研究了白细胞介素-1（IL-1），炎症性疼痛的介质，是否也在神经损伤引起的疼痛中发挥作用。用不同剂量（10-80 μg）的抗IL-1受体I（抗IL-1 RI）的大鼠单克隆中和抗体治疗一侧坐骨神经慢性缩窄性损伤的雌性C57 BL/6-小鼠（神经源性痛觉过敏和异常性疼痛的已建立模型）。该抗体剂量依赖性地减少动物中的热痛觉过敏和机械异常性疼痛。此外，在接受最高剂量抗IL-1 RI治疗的小鼠中，促炎细胞因子肿瘤坏死因子-α（TNF）的免疫反应性降低。任何治疗方案均未改变有髓纤维的变性。提示IL-1可能是神经损伤后痛觉过敏的介质。
We investigated whether interleukin-1 (IL-1), a mediator of inflammatory pain, also plays a role in pain induced by nerve injury. Female C57BL/6-mice with a chronic constrictive injury of one sciatic nerve, an established model of neurogenic hyperalgesia and allodynia, were treated with different doses (10–80 μg) of a neutralizing monoclonal rat antibody to IL-1 receptor I (anti-IL-1RI). This antibody dose-dependently reduced thermal hyperalgesia and mechanical allodynia in the animals. Furthermore, immunoreactivity for the proinflammatory cytokine tumor necrosis factor-α (TNF) was reduced in mice treated with the highest dose of anti-IL-1RI. Degeneration of myelinated fibers was not altered by any of the treatment schedules. We conclude that IL-1 may be a mediator of hyperalgesia after nerve lesion.
DOI：
10.1073/pnas.91.10.4219
发表时间：
1994-05-10
影响因子：
11.1
作者：
SCHAFER, M;CARTER, L;STEIN, C
通讯作者：
STEIN, C