【摘要】 目的　研究人参皂甙 (Ginsenosides,GS)的 3种单体成分GSRb1、Rb3 、Rg1对培养的皮层神经细胞的抗缺血效应及其机制。方法　体外培养小鼠胎鼠大脑皮层神经细胞 ,观察缺血 /再灌注对神经细胞的毒性及GSRb1、Rb3 、Rg1的保护作用。结果　培养的小鼠胎鼠大脑皮层神经细胞缺血 /再灌注损伤后 ,细胞出现明显损伤性变化 ,神经细胞活性降低 ,电镜观察显示神经细胞呈变性至坏死等不同程度的损伤 ,死亡率明显升高 ,培养上清液中乳酸脱氢酶 (LDH)释放量增加 ,而细胞匀浆中超氧化物歧化酶 (SOD)含量明显减少 ,丙二醛 (MDA)生成显著增多。GSRb1、Rb3 、Rg16 0 μmol/L能不同程度地抑制缺血 /再灌注引起的损伤性改变 ,培养上清液中LDH释放减少 ,而细胞匀浆中SOD含量明显增加 ,MDA生成显著降低。结论　 (1)GSRb1、Rb3 、Rg1对神经细胞有明显的抗缺血效应 ;(2 )GSRb1、Rb3 、Rg1抗缺血的作用机制可能与其提高神经细胞抗氧化能力、减少自由基的生成 ,保护细胞的结构与功能有关。更多还原

【Abstract】 Objective To study the neuroprotective effects and the mechanism of three monomers of Ginsenosides (GSRb 1、GSRb 3、GSRg 1) on ischemic injurie in cultured mouse cortical neurons. Methods Cytotoxicities of ischemia(6h)/reperfusion(24h) and protective effects of GSRb 1、Rb 3、Rg 1 on cultured mouse cortical neurons were observed. Results Exposure of mouse fetus cerebral cells to hypoxic/hypoglycemic medium developed a neurotoxicity expressed in the increase of LDH leakage and MDA content and the decrease of SOD content,as well as the development of morphological injury. GSRb 1、Rb 3、Rg 1(60μmol/L) significantly protected neurons against above damages. Conclusion GSRb 1,Rb 3 and Rg 1 protected cerebral cells from the injuries induced by ischemia/reperfusion via enhancing the anti-oxidative abilities,lowering the quantity of free radicals and protecting the structure and function of cells.更多还原