Oka T, Oka K, Hosoi M, Hori T
Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Brain Res. 1996 Oct 14;736(1-2):237-42. doi: 10.1016/0006-8993(96)00705-6.
The present study was undertaken to investigate whether or not the endogeneous mechanisms in the brain can modulate the changes in nociception produced by peripherally-administered interleukin-1 beta (IL-1 beta) in rats. We administered diclofenac and alpha-melanocyte-stimulating hormone (alpha-MSH) into the lateral cerebroventricle (LCV) 10 min before the intraperitoneal (i.p.) injection of recombinant human IL-1 beta (rhIL-1 beta, 1 ng/kg-100 ng/kg) and then observed the changes in nociception using a hot-plate test. The i.p. injection of rhIL-1 beta (10 ng/kg and 100 ng/kg) reduced the paw-withdrawal latency without affecting the colonic temperature. The maximal reduction in the paw-withdrawal latency was observed 30 min after the i.p. injection of rhIL-1 beta at 100 ng/kg. The rhIL-1 beta (100 ng/kg)-induced hyperalgesia was inhibited by the LCV injection of both diclofenac (1 ng) and alpha-MSH (100 ng). The LCV injection of either diclofenac (1 ng) or alpha-MSH (100 ng) was found to have no effect on nociception by itself. These findings therefore suggest that the hyperalgesia induced by peripheral IL-1 beta can be modulated by a cyclooxygenase pathway of the arachidonate and alpha-MSH in the brain.
本研究旨在探讨大鼠脑内的内源性机制是否能够调节外周给予白细胞介素-1β（IL-1β）所产生的伤害感受变化。在腹腔注射重组人IL-1β（rhIL-1β，1 ng/kg - 100 ng/kg）前10分钟，我们将双氯芬酸和α-黑素细胞刺激素（α-MSH）注入侧脑室（LCV），然后使用热板试验观察伤害感受的变化。腹腔注射rhIL-1β（10 ng/kg和100 ng/kg）可缩短爪部撤离潜伏期，而不影响结肠温度。腹腔注射100 ng/kg rhIL-1β后30分钟观察到爪部撤离潜伏期的最大缩短。双氯芬酸（1 ng）和α-MSH（100 ng）注入LCV均可抑制rhIL-1β（100 ng/kg）诱导的痛觉过敏。单独注入双氯芬酸（1 ng）或α-MSH（100 ng）到LCV对伤害感受没有影响。因此，这些发现表明，外周IL-1β诱导的痛觉过敏可被脑内花生四烯酸的环氧化酶途径和α-MSH调节。
