Department of Medical Gastroenterology C Herlev Hospital University of Copenhagen Herlev Ringvej, Herlev DK-2730 Denmark.
Mediators Inflamm. 1992;1(5):313-7. doi: 10.1155/S0962935192000462.
Melittin, the predominant fraction of bee venom proteins, was studied in an experimental model of human neutrophil granulocytes to reveal its influence on eicosanoid release, metabolism and receptor function in relation to intracellular calcium metabolism. Melittin (2 mumol/l) was as potent as the calcium ionophore A23187 (10 mumol/l) for activation of 5-lipoxygenase, releasing arachidonate only from phosphatidyl-choline and phosphatidyl-ethanolamine of cellular membranes, as judged from the decreases in radioactivity by 15.4% and 30.5%, respectively. The mechanism responsible for the release of arachidonate from cellular membranes is closely coupled to cellular calcium metabolism, and melittin was found to promote calcium entry through receptor gated calcium channels, probably due to an activation of phospholipase A(2). Furthermore, a down-regulation of leukotriene B(4) receptors was seen. The maximal number of binding sites per cell was reduced from a median of 1520 to 950 with melittin (1 mumol/l). The study has revealed some factors important for the inflammatory mechanisms mediated by melittin.
蜂毒蛋白的主要成分蜂肽在人类嗜中性粒细胞实验模型中进行了研究，以揭示其对花生四烯酸释放、代谢和受体功能的影响，以及与细胞内钙代谢的关系。蜂肽（2μmol/L）与钙离子载体 A23187（10μmol/L）一样有效激活 5-脂氧合酶，仅从细胞膜的磷脂酰胆碱和磷脂酰乙醇胺中释放花生四烯酸，分别降低放射性分别为 15.4%和 30.5%。负责从细胞膜释放花生四烯酸的机制与细胞内钙代谢密切相关，蜂肽被发现通过受体门控钙通道促进钙内流，可能是由于磷脂酶 A2 的激活。此外，还观察到白三烯 B4 受体的下调。用蜂肽（1μmol/L）处理后，每个细胞的最大结合位点数从中位数 1520 减少到 950。该研究揭示了一些与蜂肽介导的炎症机制有关的重要因素。
