摘要
实验运用离体培养的大鼠海马神经细胞,观察了过氧化氢对海马神经细胞的损伤效应及甘丙肽(GAL)对氧化应激过程中海马神经细胞的保护作用。结果显示,过氧化氢对海马神经细胞具有明显的剂量相关毒性效应。甘丙肽以及甘丙肽非特异性受体激动剂GAL1-11和甘丙肽受体2 (GalR-2)特异性激动剂GAL2-11能显著减少海马神经细胞在氧化应激过程中的损伤反应,这种效应可被GAL非特异性受体阻断剂M35阻断。实验提示GAL对氧化应激导致的海马神经细胞损伤具有保护作用,这种作用很有可能是由GalR-2受体介导。
The method of primary hippocampal nerve cell culture was used to study the injury effect of H2O2 and the protective effect of galanin(GAL) and GAL receptor agonists. Result demonstrated that H2O2 has obvious dose relative toxicity to hippocampal cells in vitro. GAL and GAL's nonselective agonist GALI-11,GaIR2's selective agonist GAL2-11 can increase the survival rate of hippocampal ceils suffered form H2O2. All the protective effects can be blocked by nonselective antagonist M35. The result indicates that GAL can protect hippocampal ceils from oxidative injury in vitro,which is most probably mediated by GaIR2.
出处
《分子细胞生物学报》
CSCD
北大核心
2006年第5期391-398,共8页
Journal of Molecular Cell Biology