Malcangio M, Bowery N G, Flower R J, Perretti M
Department of Pharmacology, School of Pharmacy, London, UK.
Eur J Pharmacol. 1996 Mar 28;299(1-3):113-8. doi: 10.1016/0014-2999(95)00845-4.
Superfusion of rat spinal cord slices with rat interleukin-1 beta resulted in a significant enhancement of electrically evoked substance P-like immunoreactivity with a maximal effect (> 2-fold increase) at 0.1 ng/ml, whereas higher concentration (10-50 ng/ml) of the cytokine inhibited (approximately 50%) the release of the neuropeptide. Interleukin-1 beta (0.1 ng/ml) potentiation of substance P-like immunoreactivity release was abrogated by co-perfusion with interleukin-1 receptor antagonist (10-100 ng/ml) or with indomethacin (1 microM). Superfusion of spinal cord with interleukin-1 beta inhibited electrically evoked calcitonin gene-related peptide-like immunoreactivity release. Modulation of substance P-like immunoreactivity release from the spinal cord by interleukin-1 beta may represent a mechanism responsible for the hyperalgesic action of the cytokine characteristic of the inflammatory response.
用大鼠白细胞介素-1β对大鼠脊髓切片进行灌流，可显著增强电诱发的P物质样免疫反应性，在0.1 ng/ml时达到最大效应（增加超过2倍），而更高浓度（10 - 50 ng/ml）的细胞因子则抑制（约50%）神经肽的释放。白细胞介素-1β（0.1 ng/ml）对P物质样免疫反应性释放的增强作用可通过与白细胞介素-1受体拮抗剂（10 - 100 ng/ml）或吲哚美辛（1 μM）共同灌流而消除。用白细胞介素-1β对脊髓进行灌流可抑制电诱发的降钙素基因相关肽样免疫反应性释放。白细胞介素-1β对脊髓P物质样免疫反应性释放的调节可能是该细胞因子在炎症反应中具有痛觉过敏作用的一种机制。
