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首页> 外文期刊>Life sciences >Induction of nociceptive responses by intrathecal injection of interleukin-1 in mice
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Induction of nociceptive responses by intrathecal injection of interleukin-1 in mice

机译：鞘内注射白细胞介素1对小鼠的伤害感受诱导。

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Intrathecal (i.t.) injection (between lumbar vertebrae 5 and 6) into mice of a markedly low dose of IL-#alpha# (3 * 10~(-4) fmol or 5.4 fg in 5 #mu#l per mouse) induced behaviors involving scratching, biting, and licking of non-stimulated hindpaws. The IL-1-induced behaviors appeared within 10 min of the injection of IL-1#alpha#, peaked at 20-40 min, and had disappeared 60 min after the injection. The IL-1-induced behaviors were similar to the nociceptive responses induced in mice by i.t. injection of substance P (SP) or subcutaneous (s.c.) injection of formalin into the footpad. The IL-1-induced behaviors were suppressed by intraperitoneal morphine, indicating that they are nociceptive responses. The nociceptive responses induced by 3 * 10~(-4) (5.4 fg) of IL-1#alpha# were almost completely suppressed by co-injection of 0.3 fmol (7.2 pg) of an IL-1 receptor antagonist (IL-1ra). An antiserum against substance P, but not an antiserum against somatostatin, suppressed the IL-1-induced nociceptive responses. The nociceptive responses induced by s.c. injeciton of 2% formalin into the footpad were also inhibited by i.t. injection of 30 pmol (720 ng) of IL-1ra. These results suggest that IL-1 may play a role in hyperalgesia in mice by acting as a factor augmenting pain transmission in the spinal cord at least in part by either directly or indirectly releasing substance P.
机译：鞘内注射（在腰椎5和6之间）明显低剂量的IL-＃alpha＃（每只小鼠5＃mu＃l中3 * 10〜（-4）fmol或5.4 fg）引起的行为涉及抓，咬和舔非刺激的后爪。 IL-1诱导的行为在注射IL-1＃alpha＃的10分钟内出现，在20-40分钟达到峰值，并在注射60分钟后消失。 IL-1诱导的行为类似于i.t.诱导的小鼠伤害感受反应。将P物质（SP）或皮下（s.c.）注射福尔马林注射到脚垫中。 IL-1诱导的行为被腹腔内吗啡抑制，表明它们是伤害性反应。通过共同注射0.3 fmol（7.2 pg）的IL-1受体拮抗剂（IL-1ra），几乎完全抑制了3 * 10〜（-4）（5.4 fg）的IL-1＃alpha＃诱导的伤害反应。 ）。针对P物质的抗血清，而非针对生长抑素的抗血清，抑制了IL-1诱导的伤害反应。 s.c.引起的伤害性反应i.t.也抑制了向足垫中注射2％福尔马林的过程。注射30 pmol（720 ng）的IL-1ra。这些结果表明，IL-1至少部分通过直接或间接释放P物质作为增加脊髓中疼痛传递的因子而在小鼠痛觉过敏中起作用。

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