低强度He-Ne激光增强牛中性粒细胞呼吸爆发的信号转导机制初探  

Primary research on signal transduction pathways involved in low intensity He-Ne laser-enhanced respiratory burst in bovine neutrophils

作　　者：池景泉[1] 刘承宜 段锐 李燕 李艳玲 

机构地区：[1]华南师范大学校医院 [2]华南师范大学传输光学实验室,广州510631

出　　处：《广东医学》2001年第10期898-899,共2页Guangdong Medical Journal

基　　金：美国激光医学学会 2 0 0 0年暑假研究基金 ;国家自然科学基金 (编号 :697780 0 3) ;教育部霍英东青年教师基金 ;广东省自然科学基金 (编号 :960 1 73)及其团队项目 (编号 :2 0 0 0 30 61 )

摘　　要：目的　研究低强度He -Ne激光增强牛中性粒细胞呼吸爆发的信号转导通路。方法　分别用酪氨酸蛋白激酶 (PTK)抑制剂genistein、磷脂酶C(PLC)抑制剂U -7312 2和蛋白激酶C(PKC)抑制剂calphostinC研究 10J/m2 He -Ne激光增强的牛中性粒细胞呼吸爆发。结果　 10J/m2 He -Ne激光增强的牛中性粒细胞呼吸爆发 ,PTK抑制剂可以完全抑制 ,PLC和PKC的抑制剂只能部分抑制。结论　PTK在低强度He -Ne激光增强牛PMN呼吸爆发过程中起着关键性的作用 ;PTK、PLC和PKC介导的信号转导途径可能参与了低强度HeObjective To study signal transduction pathways involved in low intensity He-Ne laser-enhanced respiratory burst in bovine neutrophils. Methods The protein tyrosine kinases (PTKs) inhibitor (genistein), phospholipase C (PLC) inhibitor (U-73122), and the protein kinase C (PKC) inhibitor, calphostin C, were used to probe signal transduction pathways of respiratory burst of bovine neutrophils which were induced by He-Ne laser at a dose of 10 J/m 2, respectively. Results The inhibitor of PTKs could completely inhibit the He-Ne laser-enhanced respiratory burst of neutrophils. PLC and PKC inhibitors could obviously reduce it, but not fully inhibit it. Conclusion PTKs play a key role in the He-Ne laser-enhanced respiratory burst of bovine neutrophils and signal transduction pathways mediated by PTK, PLC and PKC may be involved in this process.

关 键 词：中性粒细胞 光信号转导 低强度激光 HE-NE激光 PMN呼吸爆发 

分 类 号：R454.2[医药卫生—治疗学] R318[医药卫生—临床医学]