Genistein inhibition of OGD-induced brain neuron death correlates with its modulation of apoptosis, voltage-gated potassium and sodium currents and glutamate signal pathway
Genistein inhibition of OGD-induced brain neuron death correlates with its modulation of apoptosis, voltage-gated potassium and sodium currents and glutamate signal pathway
复制标题
金雀异黄素对 OGD 诱导的脑神经元死亡的抑制与其对细胞凋亡、电压门控钾电流和钠电流以及谷氨酸信号通路的调节相关
DOI：
10.1016/j.cbi.2016.05.033
复制
发表时间：
2016-07-25
影响因子：
5.1
通讯作者：
Liu, Yan-qiang
中科院分区：
文献类型：
--
作者：
Ma, Xue-ling;Zhang, Feng;Liu, Yan-qiang
本研究采用氧葡萄糖剥夺（oxygeneglucosedeprivation，OGD）方法建立了新生大鼠原代神经元缺氧缺血模型，观察了大豆异黄酮（genistein，genistein）对缺氧缺血神经元活力、细胞凋亡、电压激活钾（voltage-activated potassium，K-v）和钠（voltage-activated sodium，Na-v）电流以及谷氨酸受体亚基的影响。结果表明，OGD暴露降低了脑神经元的活力，增加了凋亡。同时，OGD暴露引起电压激活钾电流和钠电流的电流-电压曲线和电流幅值的变化; OGD暴露还降低了GluR 2的表达，增加了NR 2的表达。然而，染料木黄酮至少部分逆转OGD引起的影响。结果表明，缺氧缺血引起的神经元凋亡/死亡与K+外流增加、Na+内流减少、GluR 2下调和NR 2上调有关。Genistein可能通过调节K-v和Na-v电流以及GluR 2和NR 2介导的谷氨酸信号通路发挥神经保护作用。(C)2016爱思唯尔爱尔兰有限公司版权所有。
In the present study, we established an in vitro model of hypoxic-ischemia via exposing primary neurons of newborn rats to oxygeneglucose deprivation (OGD) and observing the effects of genistein, a soybean isoflavone, on hypoxic-ischemic neuron viability, apoptosis, voltage-activated potassium (K-v) and sodium (Na-v) currents, and glutamate receptor subunits. The results indicated that OGD exposure reduced the viability and increased the apoptosis of brain neurons. Meanwhile, OGD exposure caused changes in the current-voltage curves and current amplitude values of voltage-activated potassium and sodium currents; OGD exposure also decreased GluR2 expression and increased NR2 expression. However, genistein at least partially reversed the effects caused by OGD. The results suggest that hypoxic-ischemia-caused neuronal apoptosis/death is related to an increase in K+ efflux, a decrease in Na+ influx, a down-regulation of GluR2, and an up-regulation of NR2. Genistein may exert some neuroprotective effects via the modulation of K-v and Na-v currents and the glutamate signal pathway, mediated by GluR2 and NR2. (C) 2016 Elsevier Ireland Ltd. All rights reserved.