首页> 外文期刊>Journal of the Formosan Medical Association =: Taiwan yi zhi >Far-infrared ray radiation promotes neurite outgrowth of neuron-like PC12?cells through AKT1 signaling
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Far-infrared ray radiation promotes neurite outgrowth of neuron-like PC12?cells through AKT1 signaling

机译:远红外线辐射通过AKT1信号促进神经元样PC12细胞的神经突生长

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Background/purposeFar-infrared (FIR) therapy is a safe and noninvasive source for medical applications. Animal study has shown the effects of FIR in promoting nerve repair. However, the cellular mechanism is not well known. Nerve growth factor (NGF) treated neuron-like PC12?cells for neurite outgrowth have been widely employed as the in?vitro model for neural regeneration.MethodsIn this study, we tried to evaluate the potential of FIR in promoting neurite outgrowth and related mechanism by using NGF-treated neuron-like PC12?cells as a cellular model. We found that FIR could promote neurites outgrowth of neuron-like PC12?cells at earlier culture period.ResultsThe neurite outgrowth-enhancing effect of FIR irradiation was more obvious when lower NGF concentration (1?ng/ml and 10?ng/ml) was added into the medium. We also found that FIR had no thermal effects on culture medium. The effects of FIR in promoting neurite outgrowth were dose dependent, and higher power density of FIR provided more effects for improving neurite outgrowth. The mechanism of FIR in promoting neurite outgrowth was through AKT1 pathway.ConclusionThe effects of FIR irradiation on promoting neurite outgrowth and neural regeneration of NGF-treated neuron-like PC12?cells are dose dependent and through activation of AKT1 phosphorylation. This study provided important information for understanding the cellular mechanism of FIR in promoting neurite outgrowth and possible neural regeneration for further clinical applications.
机译:背景/目的远红外(FIR)治疗是医疗应用的安全且无创的来源。动物研究表明,FIR促进神经修复。但是,细胞机制尚不为人所知。神经生长因子(NGF)处理的神经元样PC12?细胞用于神经突生长的方法已广泛用作神经再生的体外模型。方法在本研究中,我们试图评估FIR促进神经突生长的潜力及其相关机制。用NGF处理的神经元样PC12细胞作为细胞模型。结果发现,在较低的NGF浓度(1?ng / ml和10?ng / ml)下,FIR可以促进神经元样PC12?细胞的神经突生长。结果表明,FIR照射的神经突生长增强作用更为明显。添加到媒体中。我们还发现,FIR对培养基没有热效应。 FIR促进神经突生长的作用是剂量依赖性的,FIR的更高功率密度为改善神经突生长提供了更多的作用。 FIR促进神经突生长的机制是通过AKT1途径进行的。结论FIR辐射对NGF处理的神经元样PC12细胞的促进神经突生长和神经再生的作用是剂量依赖性的,并且是通过激活AKT1磷酸化来实现的。这项研究为理解FIR促进神经突生长和可能的神经再生的细胞机制提供了重要的信息,以用于进一步的临床应用。

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