Department of Biomedical Engineering, School of Medicine, Keimyung University, Daegu, 42601, Korea.
Department of Medical Genetics, Hanvit Institution for Medical Genetics, Keimyung University, Daegu, 42601, Korea.
Sci Rep. 2019 Jul 12;9(1):10114. doi: 10.1038/s41598-019-46490-4.
Photobiomodulation therapy (PBMT) effects an important role in neural regeneration and function enhancement, such as expression of nerve growth factor and nerve regeneration, in neuronal tissues, and inhibition of cell death by amyloid beta in neurons is inhibited by PBMT. However, there no studies evaluated the effects of PBMT on oxidative stress in the hippocampus. The aim of this study is to evaluate the effects of PBMT on oxidative stress in the hippocampus. This study assessed the anti-oxidative effect, the expression of BDNF and antioxidant enzymes, as well as the activation of cAMP response element binding (CREB) and extracellular signal-regulated kinase (ERK) signal transduction pathways assess using a hippocampal cell line (HT-22) and mouse organotypic hippocampal tissues by PBMT (LED, 660 nm, 20 mW/cm). PBMT inhibited HT-22 cell death by oxidative stress and increased BDNF expression via ERK and CREB signaling pathway activation. In addition, PBMT increased BDNF expression in hippocampal organotypic slices and the levels of phosphorylated ERK and CREB, which were reduced by oxidative stress, as well as the expression of the antioxidant enzyme superoxide dismutase. These data demonstrate that PBMT inhibits hippocampal damage induced by oxidative stress and increases the expression of BDNF, which can be used as an alternative to treat a variety of related disorders that lead to nerve damage. Activation and redox homeostasis in neuronal cells may be a notable mechanism of the 660-nm PBMT-mediated photobioreactivity.
光生物调节疗法(PBMT)在神经元组织中对神经再生和功能增强(如神经生长因子和神经再生的表达)具有重要作用,并抑制神经元中淀粉样β对细胞死亡的抑制作用。然而,目前还没有研究评估 PBMT 对海马体氧化应激的影响。本研究旨在评估 PBMT 对海马体氧化应激的影响。本研究使用海马体细胞系(HT-22)和鼠器官型海马组织评估了 PBMT(LED,660nm,20mW/cm)对氧化应激的抗氧化作用、BDNF 和抗氧化酶的表达以及 cAMP 反应元件结合(CREB)和细胞外信号调节激酶(ERK)信号转导通路的激活作用。PBMT 抑制了由氧化应激引起的 HT-22 细胞死亡,并通过 ERK 和 CREB 信号通路的激活增加了 BDNF 的表达。此外,PBMT 增加了海马体器官型切片中的 BDNF 表达以及氧化应激导致的磷酸化 ERK 和 CREB 水平和抗氧化酶超氧化物歧化酶的表达。这些数据表明,PBMT 抑制了由氧化应激引起的海马体损伤,并增加了 BDNF 的表达,可作为治疗各种导致神经损伤的相关疾病的替代方法。神经元细胞中的激活和氧化还原稳态可能是 660nm PBMT 介导的光生物反应的一个显著机制。