Experimental Study On The Effect Of Naringin On Oxidative Stress Of Neuronal Glucose-oxygen Deprivation/reperfusion Model

Objective: To study the protective effect and possible mechanism of naringin(naringin)on nerve cells during cerebral ischemia-reperfusion injury in SD rats.Primary cerebral cortex neurons cultured in vitro with oxygen and glucose deprivation / reperfusion(OGD / Repp)model were used to explore nuclear factor E2(Nrf2)of naringin intervention in cerebral ischemia-anoxia-reperfusion injury.The effect of Nrf2 pathway on antioxidant stress To elucidate the mechanism of naringin in neuroprotective effect of cerebral ischemia reperfusion injury.Methods:1.The cultured cortical neurons in logarithmic growth stage were stained with immunofluorescence and identified.2.The cortical neurons of SD rats were used to establish OGD/Rep model.3.The cells were treated with different concentrations of NAR for 48 h.The cell activity and apoptosis were detected,and the expression of apoptosis-related protein Capase-3,bax,bcl-2,Cyt C at protein and gene level was detected.Detection of rosid MDA and GSH levels in cells of each group And SOD activity.4.Transfected si RNA-Nrf2,OENrf2 interfered with Nrf2 expression,cultured with OGD/Rep,then treated with 80 μ μ NAR for 48 h.The cellular activity and apoptosis were detected.The levels of rosid MDA and GSH and SOD activity.The nuclear transfer of Nrf2 protein,the expression of Nrf2Keap1HO-1,NOQ1 protein and gene were detected.Results: 1.Compared with the normal group,the activity of nerve cells in the model group was lower and the apoptosis rate was higher than that in the model group(P < 0.05).Compared with the model group,the neuronal activity increased and the apoptosis rate decreased in the model group,especially in the NAR-H group(P < 0.05).2.Compared with the normal group,the expression of Capase-3,bax and Cyt C in the model group was up-regulated,while the expression of bcl-2 was down regulated(P < 0.05).Compared with the model group,the expression of Capase-3,bax and Cyt C was down-regulated,while the expression of bcl-2 was up-regulated.3.After pretreatment the OGD/Rep model with NAR can upregulation of SOD1,downregulation of ROS,GSH level and MDA level.4.Compared with the model group,the neuronal activity was higher and the apoptosis rate was lower in the NAR group and OENrf2 transfection group(P < 0.05),but the contrary was found in the Nrf2-si RNA transfection group(P < 0.05).5.Compared with the model group,the level of SDS-GSH in NAR group and OENrf2 transfection group decreased significantly(P < 0.05),but there was no significant difference in Nrf2-si RNA transfection group(P > 0.05).6.Compared with model group,the expression level of Nrf2 protein in Nrf2-si RNA group was higher than that in cell nucleus(P < 0.05),while Nrf2-si RNA group was opposite(P < 0.05).7.NAR up-regulated the expression of HO-1 and NOQ1 in the downstream of Nrf2 pathway.Conclusion: Naringin can protect neurons from oxygen glucose deprivation / reperfusion by activating the antioxidant pathway mediated by Nrf2.