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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Vascular Endothelial Growth Factor Protects Cultured Rat Hippocampal Neurons Against Hypoxic Injury via an Antiexcitotoxic, Caspase-Independent Mechanism.
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Vascular Endothelial Growth Factor Protects Cultured Rat Hippocampal Neurons Against Hypoxic Injury via an Antiexcitotoxic, Caspase-Independent Mechanism.

机译:血管内皮生长因子可通过抗兴奋性毒性,胱天蛋白酶独立机制保护培养的大鼠海马神经元免受低氧损伤。

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摘要

The authors investigated the effect of vascular endothelial growth factor (VEGF) on hypoxic injury of cultured rat hippocampal neurons. Treatment with glutamate receptor antagonists prevented hypoxic neuron death. The same magnitude of protection was observed in cultures treated with VEGF, which also reduced excitotoxic neuron death induced directly by an exposure to -methyl-d-aspartate. Vascular endothelial growth factor did not alter the activation of the transcription factor nuclear factor-kappaB during hypoxia and protected cells in a PI-3-kinase-independent manner. Vascular endothelial growth factor failed to protect against staurosporine-induced, caspase-dependent apoptosis. These data suggest that VEGF-induced protection against hypoxic injury primarily involves the inhibition of excitotoxic processes.
机译:作者研究了血管内皮生长因子(VEGF)对培养的大鼠海马神经元缺氧损伤的影响。用谷氨酸受体拮抗剂治疗可预防缺氧性神经元死亡。在用VEGF处理的培养物中观察到相同程度的保护,这也减少了直接暴露于-甲基-d-天门冬氨酸引起的兴奋性毒性神经元死亡。缺氧期间,血管内皮生长因子并未改变转录因子核因子-κB的活化,并以PI-3-激酶非依赖性方式保护了细胞。血管内皮生长因子不能预防星形孢菌素诱导的胱天蛋白酶依赖性凋亡。这些数据表明,VEGF诱导的针对低氧损伤的保护作用主要涉及兴奋性毒性过程的抑制。

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