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Stem cell factor prevents neuronal cell apoptosis after acute spinal cord injury.

机译:干细胞因子可防止急性脊髓损伤后神经元细胞凋亡。

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STUDY DESIGN: A rat spinal cord injury (SCI) model and immunohistochemistry were used to examine the levels of expression of stem cell factor and c-kit. In addition, we examined whether intraperitoneal administration of stem cell factor could prevent neural cells apoptosis after acute SCI. OBJECTIVE: To evaluate the antiapoptotic effect of stem cell factor after SCI. SUMMARY OF BACKGROUND DATA: It is well known that the mode of delayed neuronal and glial cell death after SCI is apoptosis. Inhibition of apoptosis might thus promote neurologic improvement after SCI. Stem cell factor and its receptor c-kit exhibit pleiotropic effects in early hematopoiesis, and are also known to prevent hematopoietic progenitor cell apoptosis. Stem cell factor has recently been reported to be a survival factor for neural stem cells in vitro. We examined the levels of expression of stem cell factor and c-kit in normal and injured rat spinal cord. In addition, we examined whether stem cell factor prevents neural cell apoptosis after acute SCI. METHODS: We examined the expression of stem cell factor and c-kit in spinal cord after injury by quantitative RT-PCR and immunohistochemistry. Antiapoptotic effects of stem cell factor were examined using rats with SCI that received stem cell factor intraperitoneally, and were examined immunohistochemically with anticleaved PARP antibody and antiactive caspase-3 antibody between 1 and 3 days after injury. RESULTS: Upregulation of stem cell factor and c-kit expression occured after SCI. We also found that neurons express stem cell factor, and neurons and oligodendrocytes express c-kit after SCI. In addition, intraperitoneal administration of stem cell factor prevented spinal neural cells apoptosis after injury. CONCLUSION: These findings suggest the possibility that stem cell factor, a hematopoietic cytokine, could be useful as an agent for treatment of SCI.
机译:研究设计:使用大鼠脊髓损伤(SCI)模型和免疫组化方法检测干细胞因子和c-kit的表达水平。此外,我们检查了腹膜内施用干细胞因子是否可以预防急性SCI后神经细胞凋亡。目的:探讨脊髓损伤后干细胞因子的抗凋亡作用。背景数据概述:众所周知,SCI后延迟的神经元和神经胶质细胞死亡的方式是凋亡。因此,抑制细胞凋亡可能会促进SCI后神经系统的改善。干细胞因子及其受体c-kit在早期造血过程中表现出多效性作用,并且众所周知还可以防止造血祖细胞凋亡。最近有报道称干细胞因子是神经干细胞在体外的生存因子。我们检查了正常和受伤大鼠脊髓中干细胞因子和c-kit的表达水平。此外,我们检查了干细胞因子是否可预防急性SCI后神经细胞凋亡。方法:采用定量RT-PCR和免疫组化方法检测损伤后脊髓干细胞因子和c-kit的表达。使用SCI大鼠腹膜内接受干细胞因子检测干细胞因子的抗凋亡作用,并在损伤后1至3天之间用抗裂解的PARP抗体和抗活性caspase-3抗体进行免疫组织化学检查。结果:SCI后发生干细胞因子和c-kit表达上调。我们还发现SCI后神经元表达干细胞因子,神经元和少突胶质细胞表达c-kit。另外,腹膜内给予干细胞因子可防止损伤后脊髓神经细胞凋亡。结论:这些发现表明,造血细胞因子干细胞因子可作为治疗SCI的药物。

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