Ching T L, Koelemij J G, Bast A
Leiden/Amsterdam Center for Drug Research, Department of Pharmacochemistry, Vrije Universiteit Amsterdam, The Netherlands.
Inflamm Res. 1995 Mar;44(3):99-104. doi: 10.1007/BF01782018.
During an inflammation neutrophils are stimulated to produce reactive oxygen species (ROS). These ROS induce the release of histamine from mast cells, which are also present at the inflammation site. In this study dibutyryl cAMP differentiated HL60 cells are used as a model for human neutrophils. The effect of histamine on formyl-methionyl-leucyl-phenylalanine (fmlp) stimulated cells is examined. Except for histamine also an accumulation of ROS takes place at the inflammation site and we investigated if ROS can influence the response of the stimulated HL60 cells. It is found that 10(-3) M histamine can inhibit the fmlp induced superoxide anion radical production. This occurs partly via an H2 receptor because H2 antagonists like famotidine, mifentidine and ranitidine could partially antagonize this effect of histamine. When HL60 cells are exposed to hydrogen peroxide or hypochlorous acid (20 min), an increased fmlp response is found while the inhibiting effect of histamine remains unchanged.
在炎症过程中，中性粒细胞受到刺激会产生活性氧（ROS）。这些ROS会诱导肥大细胞释放组胺，肥大细胞也存在于炎症部位。在本研究中，用二丁酰环磷腺苷（dibutyryl cAMP）分化的HL60细胞作为人类中性粒细胞的模型。研究了组胺对甲酰甲硫氨酰亮氨酰苯丙氨酸（fmlp）刺激细胞的影响。除了组胺外，炎症部位还会发生ROS的积累，我们研究了ROS是否会影响受刺激的HL60细胞的反应。发现10⁻³ M组胺可抑制fmlp诱导的超氧阴离子自由基产生。这部分是通过H2受体发生的，因为法莫替丁、米芬替丁和雷尼替丁等H2拮抗剂可部分拮抗组胺的这种作用。当HL60细胞暴露于过氧化氢或次氯酸（20分钟）时，发现fmlp反应增强，而组胺的抑制作用保持不变。
