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首页> 外文期刊>Neurochemical research >Neuroprotective effects of hydroxysafflor yellow A against excitotoxic neuronal death partially through down-regulation of NR2B-containing NMDA receptors.
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Neuroprotective effects of hydroxysafflor yellow A against excitotoxic neuronal death partially through down-regulation of NR2B-containing NMDA receptors.

机译:羟基红花黄色素A对兴奋性神经元死亡的神经保护作用部分通过下调含NR2B的NMDA受体来实现。

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摘要

Hydroxysafflor yellow A (HSYA) is a component of the flower Carthamus tinctorius L. that elicits neuroprotective effects in vivo and in vitro. The purpose of this study was to investigate pharmacological properties of HSYA on neurotoxicity of glutamate in primary cultured rat cortical neurons along with its possible mechanism of action. After challenge with N-methyl-d-aspartate (NMDA, 100 microM) for 30 min, loss of cell viability and excessive apoptotic cell death were observed in cultured cortical neurons. However, the excitotoxic neuronal death was attenuated markedly by HSYA treatment. Western blot analysis revealed that HSYA decreased expression of Bax and rescued the balance of pro-and anti-apoptotic proteins. In addition, HSYA significantly reversed up-regulation of NR2B-containing NMDA receptors by exposure to NMDA, while it did not affect the expression of NR2A-containing NMDA receptors. These finding suggest that HSYA protects cortical neurons, at least partially, from inhibiting the expression NR2B-containing NMDA receptors and by regulating Bcl-2 family.
机译:羟基红花黄A(HSYA)是红花Carthhamus tinctorius L.的一种成分,在体内和体外引起神经保护作用。这项研究的目的是调查HSYA对原代培养的大鼠皮质神经元谷氨酸神经毒性的药理特性及其可能的作用机理。用N-甲基-d-天门冬氨酸(NMDA,100 microM)攻击30分钟后,在培养的皮层神经元中观察到细胞活力丧失和过度凋亡的细胞死亡。然而,HSYA治疗显着减轻了兴奋毒性神经元死亡。蛋白质印迹分析显示,HSYA降低了Bax的表达并挽救了促凋亡和抗凋亡蛋白的平衡。此外,HSYA通过暴露于NMDA可以显着逆转含NR2B的NMDA受体的上调,而它并不影响含NR2A的NMDA受体的表达。这些发现表明,HSYA至少部分地保护皮质神经元免于抑制含有NR2B的NMDA受体的表达并通过调节Bcl-2家族。

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