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Neuroprotective effects of Smad7-siRNA on oxygen-glucose deprivation (OGD) in PC12 cells

机译:Smad7-siRNA对PC12细胞氧 - 葡萄糖剥夺(OGD)的神经保护作用

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Ischemic cerebrovascular disease is a global health problem. According to the World Health Organization, ischemic stroke is actually the most common cause of death in the world. ActA/smads signaling pathways were shown to be required for the differentiation-associated physiological apoptosis of stroke. Smad7 is an important regulator of ActA/smads signaling via a negative feedback circuit but its effects have not been well understood. This experiment mainly discussed the apoptosis in ischemic cerebral injury by targeted silence smad7. In this study, we used NGF and oxygen-glucose deprivation (OGD) to stimulate PC 12 cells and convert them into neurons in order to establish an ischemia in vitro model. Combined with the small interfering technology of smad7, we took FCM and DAPI to identify apoptosis rate. These results showed that OGD 16 h apoptosis rate is 19.54%. OGD 16 h combined Smad7-siRNA apoptosis rate is 12.34 %. This results showed that the apoptosis rate was decreasing in ischemic injury when Smad7-siRNA. At the same time, it provide the reference for further study ActA/smads signaling pathways on acute ischemic brain damage.
机译:缺血性脑血管病是全球性健康问题。根据世界卫生组织的说法,缺血性卒中实际上是世界上最常见的死亡原因。显示acta / smads信号传导途径被认为是卒中的分化相关的生理凋亡。 Smad7是通过负反馈电路的Acta / Smads信号传导的重要调节器,但其效果尚未得到很好的理解。该实验主要讨论了目标沉默Smad7的缺血性脑损伤凋亡。在该研究中,我们使用NGF和氧葡萄糖剥夺(OGD)刺激PC 12细胞并将它们转化为神经元以建立体外模型的缺血。结合SMAD7的小干扰技术,我们服用了FCM和DAPI来鉴定细胞凋亡率。这些结果表明,OGD 16 H凋亡率为19.54%。 OGD 16 H组合SMAD7-siRNA凋亡率为12.34%。结果表明,当Smad7-siRNA时,凋亡率在缺血性损伤下降。同时,它为进一步研究急性缺血性脑损伤提供了进一步研究acta / smads信号传导途径的参考。

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