Hyperoside protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via nitric oxide signal pathway
Hyperoside protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via nitric oxide signal pathway
复制标题
金丝桃苷通过一氧化氮信号通路保护皮质神经元免受氧糖剥夺再灌注引起的损伤
DOI：
10.1016/j.brainres.2012.06.044
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发表时间：
2012-08-21
期刊：
影响因子：
2.9
通讯作者：
Hu, Zhuang-Li
中科院分区：
文献类型：
--
作者：
Liu, Rui-Li;Xiong, Qiu-Ju;Hu, Zhuang-Li
金丝桃苷是一种黄酮类化合物，临床上广泛用于镇痛和改善心血管功能。然而，金丝桃苷对缺血神经元的作用及其分子机制尚不清楚。本研究采用体外缺糖缺氧再灌注（OGD-R）缺血模型，观察金丝桃苷对缺血性神经元损伤的保护作用，并进一步探讨其可能的机制。结果表明，金丝桃苷对OGD-R诱导的皮层神经元损伤有保护作用，对谷氨酸诱导的神经元损伤和NMDA诱导的[Ca ~（2+）]（i）升高也有缓解作用。金丝桃苷的作用机制首先是抑制OGD-R损伤引起的CaMK Ⅱ磷酸化。同时，金丝桃苷通过抑制NF-κ B B的活化，减少OGD-R诱导的iNOS表达。此外，金丝桃苷还通过改善ERK、JNK和Bcl-2家族相关的凋亡信号通路发挥神经保护作用。综上所述，金丝桃苷对神经元缺血再灌注损伤具有保护作用，其机制可能与调节一氧化氮信号通路有关。(C)2012爱思唯尔有限公司版权所有。
Hyperoside is a flavonoid compound and widely used in clinic to relieve pain and improve cardiovascular functions. However, the effects of hyperoside on ischemic neurons and the molecular mechanisms remain unclear. Here, we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD-R) to investigate the protective effects of hyperoside on ischemic neuron injury and further explore the possible related mechanisms. Our results demonstrated that hyperoside protected cultured cortical neurons from OGD-R injury, it also relieved glutamate-induced neuronal injury and NMDA-induced [Ca2+](i) elevation. As for the mechanisms, hyperoside firstly attenuated the phosphorylation of CaMKII caused by OGD-R lesions. Meanwhile, hyperoside lessened iNOS expression induced by OGD-R via inhibition of NF-kappa B activation. Furthermore, ameliorating of ERK, JNK and Bcl-2 family-related apoptotic signaling pathways were also involved in the neuroprotection of hyperoside. Taken together, these studies revealed that hyperoside had protective effects on neuronal ischemia-reperfusion impairment, which was related to the regulation of nitric oxide signaling pathway. (C) 2012 Elsevier B.V. All rights reserved.