呋噻米对辣椒素介导的胞外信号调节激酶磷酸化的抑制作用  

INHIBITION OF FUROSEMIDE ON CAPSAICIN-INDUCED PHOSPHORYLATION OF EXTRACELLULAR SIGNAL REGULATED KINASES

作　　者：何雁冰[1] 万丽[1] 黄焕森[1] 高崇荣[1] 

机构地区：[1]广州医学院第二附属医院麻醉科,广州510260

出　　处：《中国疼痛医学杂志》2010年第1期26-29,共4页Chinese Journal of Pain Medicine

摘　　要：目的:观察阳离子-氯离子联合转运蛋白(CCC)阻断剂在辣椒素介导的胞外信号调节激酶(ERK)活化中的作用。方法:成年大鼠脊髓700μm厚切片,分成空白对照组、辣椒素组、呋噻米组、辣椒素+呋噻米组,予以相应药物处理后固定,再行冰冻切片,进行荧光免疫组化检测程序。对脊髓背角Ⅰ、Ⅱ层的磷酸化的细胞外信号传导激酶阳性(pERK IR)细胞计数,行统计学处理。结果:对照组、辣椒素组、呋噻米组、呋噻米+辣椒素组pERK阳性细胞数分别为4.19±0.42;26.83±1.14;12.31±0.90;12.14±0.72(P<0.001)。呋噻米+辣椒素组阳性细胞数比辣椒素组减少(P<0.001)。结论:呋噻米可抑制辣椒素介导的胞外信号调节激酶磷酸化,具抗伤害作用。Objective：To examine the antinociceptive action of Cation Chloride Cotransporter blocker on capsaicin-induced phosphorylation of extracellular signal-regulated kinases.Methods：The lumbar spinal cord segments of adult rats were removed,and cut to 700μm thick.The small segments were divided and put into four different solutions： solvent,capsaicin,furosemide,and furosemide plus capsaicin.After the reaction,fixed,immersed into 15% sucrose PBS in 4℃ for 24 hours.The segments were cut in a cryostat at 16μm,then processed for immunofluorescence.The numbers of immunoreactive neurons for pERK in the laminae Ⅰ、Ⅱ were counted and analyzed.Results：The numbers of immunoreactive neurons for pERK of solvent,capsaicin,furosemide,and furosemide plus capsaicin group were： 4.19±0.42;26.83±1.14;12.31±0.90;12.14±0.72（P0.001）.Furosemide significantly decreased the immunoreactive neurons caused by capsaicin（P0.001）.Conclusion：Furosemide inhibited the capsaicin-induced phosphorylation of extracellular signal-regulated kinases,and had antinociceptive effects.

关 键 词：阳离子-氯离子联合转运蛋白 胞外信号调节激酶 伤害 

分 类 号：R96[医药卫生—药理学]