细胞因子介导的炎症性痛觉过敏受白细胞介素-1受体拮抗剂的限制。
Cytokine-mediated inflammatory hyperalgesia limited by interleukin-1 receptor antagonist.
作者信息
Cunha J M, Cunha F Q, Poole S, Ferreira S H
机构信息
Department of Pharmacology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Brazil.
出版信息
Br J Pharmacol. 2000 Jul;130(6):1418-24. doi: 10.1038/sj.bjp.0703434.
Abstract
- The effect of IL-1ra on response to intraplantar (i.pl.) injection of LPS, carrageenin, bradykinin, TNFalpha, IL-1beta, IL-8, PGE(2) and dopamine was investigated in a model of mechanical hyperalgesia in rats. 2. IL-1ra inhibited hyperalgesic response to LPS, carrageenin, bradykinin, TNFalpha, and IL-1beta, but not responses to IL-8, PGE(2) and dopamine. 3. A sheep anti-rat IL-1ra serum potentiated response to LPS, carrageenin, bradykinin, TNFalpha and IL-1beta but not IL-8. 4. Carrageenin and LPS stimulated and production of immunoreactive TNFalpha, IL-1beta and IL-1ra in the skin of injected paws. 5. The inhibition by IL-1ra of the hyperalgesic response to carrageenin was not affected by antibodies neutralizing IL-4 and IL-10. 6. In mice, IL-1ra inhibited the nociceptive response to i.p. injection of acetic acid. 7. These data suggest that IL-1ra, released at sites of inflammation, limits inflammatory hyperalgesia. This effect is independent of (IL-1ra-induced) IL-4 and IL-10 and appears to be the result of antagonism by IL-1ra of IL-1beta-stimulated eicosanoid production.
摘要
- 在大鼠机械性痛觉过敏模型中，研究了白细胞介素-1受体拮抗剂（IL-1ra）对足底注射脂多糖（LPS）、角叉菜胶、缓激肽、肿瘤坏死因子α（TNFα）、白细胞介素-1β（IL-1β）、白细胞介素-8（IL-8）、前列腺素E2（PGE2）和多巴胺的反应的影响。2. IL-1ra抑制对LPS、角叉菜胶、缓激肽、TNFα和IL-1β的痛觉过敏反应，但不抑制对IL-8、PGE2和多巴胺的反应。3. 羊抗大鼠IL-1ra血清增强了对LPS、角叉菜胶、缓激肽、TNFα和IL-1β的反应，但不增强对IL-8的反应。4. 角叉菜胶和LPS刺激注射爪皮肤中免疫反应性TNFα、IL-1β和IL-1ra的产生。5. IL-1ra对角叉菜胶痛觉过敏反应的抑制不受中和IL-4和IL-10的抗体的影响。6. 在小鼠中，IL-1ra抑制腹腔注射乙酸的伤害性反应。7. 这些数据表明，在炎症部位释放的IL-1ra限制炎症性痛觉过敏。这种作用独立于（IL-1ra诱导的）IL-4和IL-10，似乎是IL-1ra拮抗IL-1β刺激的类花生酸产生的结果。
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