Ohsaka A, Saionji K, Sato N, Igari J
Department of Internal Medicine, Hitachi General Hospital, Ibaraki, Japan.
Exp Hematol. 1994 May;22(5):460-6.
Recombinant human granulocyte colony-stimulating factor (rhG-CSF) enhanced superoxide (O2-) release in human neutrophils stimulated by the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) and inversely regulated the surface expression of cellular adhesion molecules, leukocyte adhesion molecule-1 (LAM-1) and CD11b/CD18 leukocyte integrin, on human neutrophils; that is, rhG-CSF downregulated the expression of LAM-1 and upregulated the expression of CD11b on neutrophils. The cationic local anesthetic lidocaine inhibited not only FMLP-induced O2- release in neutrophils but also FMLP-induced CD11b upregulation and LAM-1 downregulation on neutrophils in a dose-dependent manner. Lidocaine also abolished the priming effect of rhG-CSF for enhanced release of O2- in neutrophils and inhibited rhG-CSF-induced CD11b upregulation and LAM-1 downregulation on neutrophils in a dose-dependent manner. These findings suggest that lidocaine inhibits human neutrophil functions, such as adherence to endothelial cells, by interfering with the expression of cellular adhesion molecules on neutrophils, and that lidocaine might have anti-inflammatory properties by inhibiting the effect of inflammatory cytokines.
重组人粒细胞集落刺激因子（rhG-CSF）可增强趋化肽N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（FMLP）刺激的人中性粒细胞中超氧化物（O2-）的释放，并反向调节人中性粒细胞上细胞黏附分子、白细胞黏附分子-1（LAM-1）和CD11b/CD18白细胞整合素的表面表达；也就是说，rhG-CSF下调中性粒细胞上LAM-1的表达并上调CD11b的表达。阳离子局部麻醉药利多卡因不仅剂量依赖性地抑制FMLP诱导的中性粒细胞中O2-的释放，还剂量依赖性地抑制FMLP诱导的中性粒细胞上CD11b上调和LAM-1下调。利多卡因还消除了rhG-CSF对增强中性粒细胞中O2-释放的启动作用，并剂量依赖性地抑制rhG-CSF诱导的中性粒细胞上CD11b上调和LAM-1下调。这些发现表明，利多卡因通过干扰中性粒细胞上细胞黏附分子的表达来抑制人中性粒细胞功能，如对内皮细胞的黏附，并且利多卡因可能通过抑制炎性细胞因子的作用而具有抗炎特性。
