【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。更多还原

【Abstract】 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 PI3 K/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 EB25 μg/mL group and the EB50 μg/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 EB25 μg/mL group and the EB50 μg/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 PI3 K/Akt signaling pathway and inhibiting neuronal apoptosis.更多还原