Effects Of GM-1 On Primary Cultured Rat's Neurons Apoptosis Induced By Ischemia-like

Objective: To investigate the damage of ischemia-like-reperfusion on the primary cultured rat's cortical neurons and the protective effects of GM-1.Methods:Cortical neurons cultured for 7 days were randomly divided into three groups:control group,ischemia-like-reperfusion group and plus GM-1group treated. Cortical neurons were exposed to ischemia-like environment for 30min and then cultured for 1h 6h 12h 24h under normoxic condition.Then morphology of nerurons was observed under inverted microscope.The survival rates of neurons at different culture times were compared by MTT colonmetry. The apoptosis of neurons was detected with the method of microscope and the apoptotic rate of neurons was measured using flow cytometry. Statistical analysis were using SPSS12.0 software.Comparision among groups were performed by using t-test and SNK-test.P<0.05 is significant.Results: We established a experimented cultured rat's cortical neurons by using the common culture methord.The cortical neurons was detected by neuronal specific enolase(NSE) immunocytochemical staining.We established a model by the mothed of ischemia-like-reperfusion on the cortial neurons.Before the ischemia(the normal neurons),the MTT colonmetry,the stain of apoptosis neurons and the apoptotic rate of neurons using flow cytometry of three groups were no deference(P>0.05).It proved that the followed experiment was truly and confidence.After ischemia-like-reperfusion,at different times,the ischemia-like-reperfusion group and plus GM-1 group were significant difference in MTT colonmetry,the stain of apoptosis neurons and the apoptotic rate of neurons using flow cytometry.Conclusion Ischemia-like-reperfusion could lead to increasing apoptosis and death of rate cortical neurons.:GM-1 can ameliorate the toxicity damage of neurons caused by ischemia-like-reperfusion through reducing neuron apoptosis, and increase the survival rate of neurons which suggests that GM-1 could protect rat's cortical neurons from damage under ischemia-like condion.