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白细胞介素-1β增强辣椒素诱导的大鼠皮肤神经源性血管舒张。

Interleukin-1 beta enhances capsaicin-induced neurogenic vasodilatation in the rat skin.

作者信息

Herbert M K, Holzer P

机构信息

Department of Anaesthesiology, University of Würzburg, Germany.

出版信息

Br J Pharmacol. 1994 Mar;111(3):681-6. doi: 10.1111/j.1476-5381.1994.tb14791.x.

Abstract
  1. This study examined the effect of interleukin-1 beta (IL-1 beta) on the capsaicin-induced increase in cutaneous blood flow of anaesthetized rats as measured by laser Doppler flowmetry. 2. The substances were administered by intraplantar subcutaneous injection of 10 microliters-volumes, saline being injected into one hindpaw and IL-1 beta into the other. 3. IL-1 beta (0.5-500 pg) was without effect on blood flow on its own but dose-dependently enhanced the hyperaemic response to intraplantar capsaicin (0.3 microgram) up to 180% (P < 0.05) of the response seen in saline-treated paws. 4. Il-1 beta-(163-171), a fragment devoid of proinflammatory activity, failed to enhance capsaicin-induced hyperaemia when given at a dose of 50 pg. 5. Indomethacin (10 mg kg-1, i.p.) did not alter the capsaicin-induced vasodilatation but prevented IL-1 beta (50 pg) from augmenting the hyperaemic response to capsaicin. 6. The hyperaemia evoked by intraplantar calcitonin gene-related peptide (0.038-3.8 ng) was not altered by IL-1 beta (50 pg). 7. These data indicate that IL-1 beta enhances the cutaneous hyperaemic response to afferent nerve stimulation with capsaicin in a prostaglandin-dependent manner. This proinflammatory action of the cytokine appears to arise from sensitization of afferent nerve endings.
摘要
  1. 本研究通过激光多普勒血流仪检测了白细胞介素-1β(IL-1β)对辣椒素诱导的麻醉大鼠皮肤血流量增加的影响。2. 通过足底皮下注射10微升体积的物质,将生理盐水注入一侧后爪,将IL-1β注入另一侧。3. IL-1β(0.5 - 500皮克)单独对血流量无影响,但剂量依赖性地增强了对足底注射辣椒素(0.3微克)的充血反应,最高可达生理盐水处理爪中所见反应的180%(P < 0.05)。4. Il-1β-(163 - 171),一种缺乏促炎活性的片段,以50皮克的剂量给药时未能增强辣椒素诱导的充血。5. 吲哚美辛(10毫克/千克,腹腔注射)未改变辣椒素诱导的血管舒张,但阻止了IL-1β(50皮克)增强对辣椒素的充血反应。6. 足底注射降钙素基因相关肽(0.038 - 3.8纳克)引起的充血未被IL-1β(50皮克)改变。7. 这些数据表明,IL-1β以前列腺素依赖的方式增强了对辣椒素传入神经刺激的皮肤充血反应。这种细胞因子的促炎作用似乎源于传入神经末梢的致敏。

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