Kanbara T, Tomoda M K, Sato E F, Ueda W, Manabe M
Department of Anesthesiology and Resuscitology, Kochi Medical School, Japan.
Biochem Pharmacol. 1993 Apr 22;45(8):1593-8. doi: 10.1016/0006-2952(93)90299-c.
The addition of agents, such as tumor necrosis factor-alpha, to human peripheral neutrophils (HPPMN) induces priming, which enhances the receptor-mediated superoxide (O2-) generation and tyrosine phosphorylation of several HPPMN proteins. Lidocaine, a local anesthetic, inhibited both enhanced O2- generation and tyrosine phosphorylation of a 115 kDa protein in a concentration- and time-dependent manner. Lidocaine also inhibited protein kinase C sensitive O2- generation induced by phorbol myristate acetate, but not time dependently. Furthermore, lidocaine inhibited O2- generation by non-primed HPPMN induced by formylmethionyl-leucyl-phenylalanine, but this inhibition needed a higher concentration of lidocaine compared with that of primed HPPMN. These results suggest that lidocaine inhibits the priming step of neutrophil activation and that it is linked to the inhibition of tyrosine phosphorylation of a 115 kDa protein.
向人外周血中性粒细胞（HPPMN）中添加诸如肿瘤坏死因子-α等因子会诱导启动，这会增强受体介导的超氧化物（O2-）生成以及几种HPPMN蛋白的酪氨酸磷酸化。局部麻醉剂利多卡因以浓度和时间依赖性方式抑制增强的O2-生成和115 kDa蛋白的酪氨酸磷酸化。利多卡因还抑制佛波酯肉豆蔻酸酯乙酸盐诱导的蛋白激酶C敏感的O2-生成，但不具有时间依赖性。此外，利多卡因抑制甲酰甲硫氨酰-亮氨酰-苯丙氨酸诱导的未启动的HPPMN的O2-生成，但与启动的HPPMN相比，这种抑制需要更高浓度的利多卡因。这些结果表明，利多卡因抑制中性粒细胞激活的启动步骤，并且这与抑制115 kDa蛋白的酪氨酸磷酸化有关。
