论文部分内容阅读
目的研究一氧化氮—环鸟苷酸 (NO cGMP)通路与鼠小脑颗粒细胞 (CGC)存活的相关性。方法通过光学显微镜观察N -甲基 -D -天门冬氨酸 (NMDA) ,一氧化氮释放剂 2’ ,2’ (hydrox ynitrosohydrazono)bisethanamine(Deta NONOate)和环鸟苷酸类物质 8 溴鸟苷 3’ ,5’ 环单磷酸 (cGMP)通过NO cGMP通路而对CGC存活所产生的影响 ,以及一氧化氮酶抑制剂NG 硝基 L 精氨酸 (NAME) ,可溶性鸟苷酰环化酶抑制剂 6 Anilinoquinoline 5 ,8 quinolinedione(LY835 83) ,环鸟苷酸蛋白激酶G抑制剂Guanosine 3’ ,5’ cyclicmonophosphorothioate ,8 (4 Chlorophenylthio) ,Rp Isomer,Triethylammoniumsalt(Rp 8 pCPT cGMPS)对通路的阻断作用。结果NMDA ,Deta NONOate和cGMP均能在无酒精的环境下 ,促进细胞的生存。并能不同程度地对CGC产生保护作用 ,减轻酒精对细胞的毒性作用。但NAME和LY835 83却分别能抑制NMDA和Deta NONOate的作用 ,而Rp 8 pCPT cGMPS则能消除cGMP对细胞的影响。结论NO cGMP通路在促进鼠小脑颗粒细胞的存活和抵抗酒精的神经毒性过程中起到关键的作用
Objective To investigate the relationship between NO cGMP pathway and the survival of rat cerebellar granulosa cells (CGCs). Methods The inhibitory effects of N - methyl - D - aspartate (NMDA), nitric oxide releasing agent 2 ’, 2’ (hydroxynitrosohydrazono) bisethanamine (Deta NONOate) and cyclic guanosine 8 bromoguanidine The effects of 3 ’, 5’ -cyclic monophosphate (cGMP) on the viability of CGCs via the NO cGMP pathway, as well as the effects of the nitric oxide enzyme inhibitor NG nitro L arginine (NAME), soluble guanylyl cyclase inhibition Agent 6 Anilinoquinoline 5, 8 quinolinedione (LY835 83), Blocking of the pathway by the cGMP inhibitor Guanosine 3 ’, 5’ cyclicmonophosphorothioate, 8 (4 Chlorophenylthio), Rp Isomer, Triethylammonium salt (Rp 8 pCPT cGMPS) effect. Results NMDA, Deta NONOate and cGMP both promoted cell survival in a non-alcoholic environment. And to varying degrees, have a protective effect on CGC, reduce the toxic effects of alcohol on cells. However, NAME and LY835 83, respectively, inhibited the effects of NMDA and Deta NONOate, whereas Rp 8 pCPT cGMPS eliminated the effect of cGMP on cells. Conclusions The NO cGMP pathway plays a key role in promoting the survival of rat cerebellar granule cells and in counteracting the neurotoxicity of alcohol