不同作用机制的镇痛药对细胞缝隙连接通道蛋白Cx43的作用

Effects of Different Analgesics on Gap Junction Protein Cx43

【目的】探讨不同作用机制的镇痛药对细胞缝隙连接通道功能的作用。【方法】天然表达Cx43的小鼠睾丸支持细胞TM4实验前用细胞诱导培养液培养使其表达形成有效的细胞缝隙连接(GJ),细胞接种荧光示踪法测定镇痛药对表达Cx43的TM4细胞GJ功能的影响,同时Westernblot检测细胞缝隙连接通道蛋白之一Cx43的表达。【结果】吗啡不影响TM4细胞中Cx43的GJ功能,曲马多和凯纷均抑制TM4细胞中Cx43的的GJ功能,但均不影响Cx43的表达。【结论】曲马多和凯纷均抑制由Cx43组成的细胞缝隙连接功能,提示了一个新的镇痛机制:即曲马多和凯纷可能通过抑制中枢神经元的GJ产生镇痛作用。

【Objective】 This study was designed to investigate the effects of analgesics with different mechnism on cell gap junction （GJ） function. Mouse TM4 cells expressing Cx43 were cultured with medium to inducing effective GJ.【Methods】The role of gap junctions in the modulation of TM4 cell line expressing Cx43 was explored by ＂Parachute＂ dye-coupling assay. Cx43 protein expression was detected by Western blot. 【Results】 Tramadol and flurbiprofen,but not Morphine,significantly reduced Cx 43 gap junction function,however this effect could not regulate Cx43 protein expression. 【Conclusion】 The results suggest that Tramadol and flurbiprofen depress function of Cx 43 gap junction activity,and Morphine have no effect on this gap junction. Tramadol and flurbiprofen inhibit the central nerve GJ to produce analgesia.