摘要
目的探讨刺五加苷B(EB)对缺氧/复氧诱导的SD大鼠皮层神经元损伤的保护作用及其对PI3K/Akt信号通路的影响。方法将原代培养的SD大鼠皮层神经元随机分为Control组、H4h/R24h组、EB25μg/mL组和EB50μg/mL组4组。H4h/R24h组建立缺氧/复氧模型;EB25μg/mL组和EB50μg/mL组则先用EB预保护3h后再造模。采用CCK-8法测定神经元的细胞活力,TUNEL法检测神经元的凋亡率,Western blotting法检测神经元中cleaved-Caspase-3、Bax、Bcl-2、Akt和p-Akt蛋白表达水平。结果与Control组比较,H4h/R24h组神经元细胞活力降低,凋亡率、cleaved-Caspase-3和p-Akt蛋白表达水平以及Bax/Bcl-2比值均升高(P<0.01)。与H4h/R24h组比较,EB25μg/mL组和EB50μg/mL组神经元细胞活力均增高,凋亡率、cleaved-Caspase-3蛋白表达水平和Bax/Bcl-2比值均降低(P均<0.05);神经元p-Akt蛋白表达水平均升高(P<0.05)。结论EB对缺氧/复氧诱导的SD大鼠皮层神经元损伤具有神经保护作用,其作用机制可能与促进PI3K/Akt信号通路的激活而抑制神经元凋亡有关。
Objective To investigate the protective efficacy of eleutheroside B(EB)on cortical neuron injury induced by hypoxia/reoxygenation in SD rats and the impact on PI3K/Akt signaling pathway.Methods The primary cultured cortical neurons of SD rats were randomly divided into the control group,the H4 h/R24 h group,the EB25μg/mL group and the EB 50μg/mL group.The hypoxia/reoxygenation model was established in the H4 h/R24 h group.The EB25μg/mL group and the EB50μg/mL group were pre-protected with EB for 3 hours before the model was established.The cell viability of neurons was detected by CCK-8 method,the apoptosis rate of neurons was detected by TUNEL method,and the expression levels of cleaved-Caspase-3,Bax,Bcl-2,Akt and p-Akt protein in neurons were detected by Western blotting method.Results Compared with the control group,the cell viability of neurons in the H4 h/R24 h group decreased,and the apoptosis rate,the expression levels of cleaved-Caspase-3 and p-Akt protein and the ratio of Bax/Bcl-2 all increased(P<0.01).Compared with the H4 h/R24 h group,the cell viability of neurons in the EB25μg/mL group and the EB50μg/mL group both increased,while the apoptosis rate,expression levels of cleaved-Caspase-3 protein and the ratio of Bax/Bcl-2 all decreased(P<0.05).The expression level of p-Akt protein in neurons increased(P<0.05).Conclusion There is neuroprotective efficacy in EB on cortical neuron injury induced by hypoxia/reoxygenation in SD rats,and the mechanism may be related to promoting the activation of PI3K/Akt signaling pathway and inhibiting neuronal apoptosis.
作者
邓凤春
王滨
沈云虹
金香兰
赵红晔
DENG Fengchun;WANG Bin;SHEN Yunhong;JIN Xianglan;ZHAO Hongye(Section of Teaching and Research in Anatomy,Qiqihar Medical University,Heilongjiang,Qiqihar 161006,China;Section of Teaching and Research in Physiology,Qiqihar Medical University,Heilongjiang,Qiqihar 161006,China)
出处
《中国医药科学》
2020年第21期27-30,66,共5页
China Medicine And Pharmacy
基金
黑龙江省齐齐哈尔市科学技术计划项目(SFGG-201761)。
