| Objective: To study the neruoprotective effects of three monomers of Ginsenosides (GSRbi, GSRb3 GSRgi) on ischemic injuries in cultured mouse cortical neurons.Methods: (1)Morphological observation and MTT assay were used to compare the effects of different duration of ischemia on cultured mouse cortical neurons.(2)Various concentrations of GSRb1 Rb3 Rg1 (20 -100u mol/100ml) were used to observe their effects on ischemic cultured mouse cortical neurons and neuronal viabilities in primary cultures from mouse cerebral cortex assessed by means of MTT assay. (3)The ischemic model of cerebral cortex neuron culture was used. The protective effects of GSRb Rb3 Rg1 on mouse cultured cortical neurons were investigated by morphological observation1 biochemical analysis and neuronal Apoptotic rate.Results: (1)The neuronal viability decreased or the cell death rate increased as ischemia duration prolonged .(2)GSRb1 Rb3 Rg1 could improve the neuronal viability respectively in a dose dependent manner in the range of 20 to 60 u mol/100ml.These effects were most significant at the concentration 60 mol/100ml. While in the range of 60 to 100 u mol/100ml, the protective effects of GS decreased. GSRb1 Rb3 Rg1 at 100u mol/lOOml had no protective effects.(3)Compared with ischemia group, The cell death rate decreased significantly together with decreasing in LDH release No releasex mDA content and cell apoptotic rate , and the superoxide dismutase (SOD) activity increased significantlyin the study group(p<0.05 & p<0.01) after being treated with GS at 60 u mol/100ml. By using scanning electronic microscope and electromicroscopy, morphological injury was abated markedly and some neurous shape was resume to normal in the study group treated with GS.Conclusion: GSRbi Rb3 Rgi may protect ischemic mouse cortex neurons by increasing the content of SOD, inhibiting lipid peroxiolation and protecting brain from the excitatory toxicity of excitatory ami no acid (EAA).
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