Neuropsychopharmacology and Toxicology Program, BK21 PLUS Project, College of Pharmacy, Kangwon National University, Chunchon, Republic of Korea.
College of Forest and Environmental Sciences, Kangwon National University, Chunchon, 24341, Republic of Korea.
Neurochem Int. 2019 Jan;122:144-148. doi: 10.1016/j.neuint.2018.11.019. Epub 2018 Nov 28.
Compelling evidence suggests that far-infrared ray (FIR) possesses beneficial effects on emotional disorders. However, the underlying mechanism conveyed by FIR remains unclear. Recently, we demonstrated that exposure to FIR induces antioxidant potentials via up-regulation of glutathione peroxidase (GPx)-1 gene. The antioxidant potentials might be important for the modulation on the neuropsychotoxic conditions. Exposure to FIR protects from methamphetamine (MA)-induced memory impairments via phosphorylation of ERK signaling by positive modulation of protein kinase C δ (PKCδ), M1 muscarinic acetylcholine receptor (M1 mAChR), and nuclear factor E2-related factor 2 (Nrf2) transcription factor. In addition, exposure to FIR positively modulates MA-induced behavioral sensitization via attenuating mitochondrial dysfunction by down-regulation of dopamine D1 receptor. In this mini-review, we have discussed with the protective potentials mediated by FIR against MA-induced psychotoxic burdens.
有强有力的证据表明,远红外线(FIR)对情绪障碍有有益的影响。然而,FIR 所传达的潜在机制尚不清楚。最近,我们证明,暴露于 FIR 会通过上调谷胱甘肽过氧化物酶 (GPx)-1 基因来诱导抗氧化潜力。抗氧化潜力对于调节神经精神毒性条件可能很重要。暴露于 FIR 通过正调控蛋白激酶 C δ (PKCδ)、M1 毒蕈碱乙酰胆碱受体 (M1 mAChR) 和核因子 E2 相关因子 2 (Nrf2) 转录因子来磷酸化 ERK 信号,从而防止甲基苯丙胺 (MA) 引起的记忆损伤。此外,暴露于 FIR 通过下调多巴胺 D1 受体来减轻线粒体功能障碍,从而积极调节 MA 诱导的行为敏化。在这篇简要综述中,我们讨论了 FIR 对 MA 引起的精神毒性负担的保护潜力。