纳洛酮在细胞信号转导系统中对甲硫氨酸脑啡肽的拮抗作用

The role of naloxone against methionine-enkephalin on signal transduction sys- tem in mouse NS-1 cells

目的:探讨甲硫氨酸脑啡肽对细胞信号转导系统的影响及其机制。方法:用甲硫氨酸脑啡肽及不同浓度的纳洛酮处理小鼠的骨髓瘤细胞(NS-1),采用组蛋白磷酸化法测定NS-1细胞蛋白激酶A(PKA)和蛋白激酶C(PKC)的活性。结果:1×10-6mol／L的甲硫氨酸脑啡肽可以升高NS-1细胞胞浆PKA活性,却降低胞浆PKC活性,而且这2种作用均能被不同浓度的纳洛酮所拮抗。结论:甲硫氨酸脑啡肽通过传统的阿片受体机制参与了2条(cAMP-PKA途径及DG-PKC途径)胞外信号传递系统的信号传递。

Objective： To study the effects and mechanisms of methionine-enkephalin on the signal transduction system. Methods： The mouse NS-1 cells were treated with methionine-enkephalin （MENK）and different concentrations of naloxone. The activities of protein kinase A （PKA） and protein kinase C （PKC） in the NS-1 cells were measured by phosphoration of histone. Results： MENK at a concentration of 1×10^-6mol/L could enhance the activity of PKA and decrease the activity of PKC in cytoplasm of NS-1 cells, which were antagonized by the naloxone. Conclusion： It might be infered that two signal transduction systems （cAMP-PKA route and DG-PKC route） were involved in the effect of MENK by binding traditional opioid receptors and therefore resulted in different biological effects.