右美沙芬对培养海马神经元缺氧损伤的保护作用及对Bcl-2表达的研究

目的　观察谷氨酸NMDA受体拮抗剂右美沙芬对体外培养海马神经元缺氧损伤的保护作用及对Bcl 2表达的影响。方法　以不同浓度 (10、5 0及 10 0 μmol L)的右美沙芬处理培养的大鼠海马神经元 ,10min后给予缺氧处理4h。停止处理后 2 4h ,以细胞存活率、乳酸脱氢酶 (LDH)流出量和Bcl 2免疫阳性细胞表达为指标进行观察。结果与正常对照组比较 ,缺氧损伤使细胞存活率下降、LDH流出量增加、Bcl 2免疫阳性细胞减少 (P <0 .0 5 ) ;而右美沙芬组与缺氧组相比细胞存活率改善、LDH流出量减少、Bcl 2免疫阳性细胞增加 (P <0 .0 5 )。结论　右美沙芬对体外培养海马神经元缺氧损伤具有保护作用 ,其机制可能与阻止由损伤引起的Bcl 2蛋白表达下调有关。

The protective action of dextromethorphan against anoxic damage of cultured hippocampal neurons and study on the changes of Bcl-2 expression

Objective To study the effect of dextromethorphan (DM) on Bcl-2 expression in cultured hippocampal neurons with anoxic damage.Methods Cultured hippocampal neurons were pre-treated with various concentrations of DM (10、50、100 μmol/L) for 10 min,then subjected to anoxia for 4 hours.After 24 hours,cell survival rate,efflux of lactate dehydrogenase (LDH) and immunohistochemical examination of Bcl-2 were investigated.Results Anoxia reduced cell survival rate,increased efflux of LDH and decreased Bcl-2 expression.However,neurons exposed to anoxia plus DM showed improved cell survival,less efflux of LDH and increased Bcl-2 expression (P<0.05).Conclusion DM was able to protect cultured hippocampal neurons against anoxic damage,probably through blocking the down-regulation of Bcl-2 expression by anoxic damage.