PHARMACOLOGICAL EVIDENCE FOR A ROLE OF LIPOXYGENASE PRODUCTS IN PLATELET-ACTIVATING-FACTOR (PAF)-INDUCED HYPERALGESIA
PHARMACOLOGICAL EVIDENCE FOR A ROLE OF LIPOXYGENASE PRODUCTS IN PLATELET-ACTIVATING-FACTOR (PAF)-INDUCED HYPERALGESIA
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DOI：
10.1016/0006-2952(87)90633-2
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发表时间：
1987-10-01
影响因子：
5.8
通讯作者：
GOLDENBERG, MM
中科院分区：
文献类型：
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作者：
DALLOB, A;GUINDON, Y;GOLDENBERG, MM
血小板活化因子（PAF）是一种强有力的炎症介质，可降低大鼠后爪的伤害性感受阈值。疼痛的敏感性，测量所施加的压力，诱导发声，增加最大的合成PAF注射后3和4小时。PAF引起的痛觉过敏反应被花生四烯酸代谢的脂氧合酶途径干扰剂特异性抑制，而不受环氧合酶抑制剂的影响。BW-755C（3-30 mg/kg，p.o.）和L-615，919（0.01-0.3 mg/kg，p.o.）显着降低PAF诱导的痛觉过敏，而吲哚美辛没有效果。L-615，919是一种特异性5-脂氧合酶抑制剂，是这种痛觉过敏模型的有效抑制剂，这一发现导致人们推测白三烯是炎性疼痛的重要介质。
Platelet-activating factor (PAF), a potent inflammatory mediator, decrease the nociceptive threshold in the rat hindpaw. Pain sensitivity, measured by the applied pressure necessary to induce vocalization, was increased maximally at 3 and 4 hr after injection of synthetic PAF. The hyperalgesic response to PAF was specifically inhibited by agents that interfere with the lipoxygenase pathway of arachidonic acid metabolism and was not affected by cyclooxygenase inhibitors. BW-755C (3-30 mg/kg, p.o.) and L-615,919 (0.01-0.3 mg/kg, p.o.) significantly reduced PAF-induced hyperalgesia, whereas indomethacin had no effect. The finding that L-615,919, a specific 5-lipoxygenase inhibitor, was a potent inhibitor of this model of hyperalgesia leads to speculation that leukotrienes are important mediators of inflammatory pain.