【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。更多还原

【Abstract】 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(P<0.001).Furosemide significantly decreased the immunoreactive neurons caused by capsaicin(P<0.001).Conclusion:Furosemide inhibited the capsaicin-induced phosphorylation of extracellular signal-regulated kinases,and had antinociceptive effects.更多还原