Priming effect of substance Ponsuper oxideanionradical production inhumanneu trophils

神经肽Ｐ物质能激活多种参与炎症和免疫反应的细胞．然而Ｐ物质直接刺激人粒细胞产生超氧阴离子（Ｏ÷２）需要较高的浓度（＞１０μｍｏｌ·Ｌ－１）．本实验观察了低浓度Ｐ物质对人粒细胞超氧阴离子生成的活化作用．结果表明，Ｐ物质在低浓度时（３μｍｏｌ·Ｌ－１）能活化人粒细胞，使甲酰基－甲硫氨酰基－亮氨酰基苯丙氨酸（ｆＭＬＰ）刺激产生的超氧阴离子明显增多．Ｐ物质的这一活化作用呈剂量和时间依赖性．在无细胞外钙的情况下，Ｐ物质没有这种活化作用．Ｐ物质活化ｆＭＬＰ引起的Ｏ÷２生成增多作用可被神经激肽（ＮＫ）－１受体阻断剂ｓｐｅｎｔｉｄｅ（１μｍｏｌ·Ｌ－１），磷脂酶Ｃ抑制剂Ｕ－７３１２２（１０ｎｍｏｌ·Ｌ－１）以及Ｃａ２＋通道阻断剂尼卡地平（１μｍｏｌ·Ｌ－１）所抑制．这些发现提示，Ｐ物质活化人粒细胞可能是经ＮＫ－１受体偶联的磷脂酰肌醇代谢途径，并且是细胞外钙依赖性的

Priming effect of substance P on superoxide anion radical production in human neutrophils

The neuropeptide substance P (SP) can activate cell types involved in inflammatory processes. However, stimulation of human neutrophils by SP to produce superoxide anion radical (O ÷ 2 ) requires even higher concentration (>10 μmol·L -1 ). In this experiment, we studied the priming effect of SP on superoxide anion radical production in human neutrophils. Our results shows that SP in lower concentration (3 μmol·L -1 ) could prime formyl-methionyl- leucyl-phenylalanine(fMLP)-induced O ÷ 2 production and the priming effect of SP was dose-and time-dependent. The SP-induced priming effect was not observed in the absence of extracellular Ca 2+ ([Ca 2+ ] o ). The SP- primed O ÷ 2 responses to fMLP (3 nmol·L -1 ) stimulation was inhibited by the neurokinin-1 (NK-1) receptor antagonist spentide (1 μmol·L -1 ), the specific phospholipase C (PLC) inhibitor U-73122 (10 nmol·L -1 ) and the Ca 2+ channel antagonist nicardipine (1 μmol·L -1 ). These findings suggest that SP primes neutrophils presumably through the NK-1 receptor linked phosphatidyl inositol response and in extracellular Ca 2+ -dependent manner.