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Curr Neuropharmacol. 2019 Feb 27. doi: 10.2174/1570159X17666190228114318. [Epub ahead of print]

Far-infrared ray-mediated antioxidant potentials are important for attenuating psychotoxic disorders.

Author information

1
Neuropsychopharmacology and Toxicology Program, BK21 PLUS Project, College of Pharmacy, Kangwon National University, Chunchon 24341. Korea.
2
College of Forest and Environmental Sciences, Kangwon National University, Chunchon 24341. Korea.
3
Department of Internal Medicine, Medical School, Kangwon National University, Chunchon 24341. Korea.
4
Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul 06974. Korea.
5
Department of Pharmacology, School of Pharmacy, Sungkyunkwan University Suwon 16419. Korea.
6
Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine and Bio/Molecular Informatics Center, Konkuk University, Seoul. Korea.

Abstract

Far-infrared ray (FIR) is an electromagnetic wave that produces various health benefits against pathophysiological conditions, such as diabetes mellitus, renocardiovascular disorders, stress, and depression etc. However, the therapeutic application on the FIR-mediated protective potentials remains to be further extended. To achieve the better understanding on FIR-mediated therapeutic potentials, we summarized additional findings in the present study that exposure to FIR ameliorates stressful condition, memory impairments, drug dependence, and mitochondrial dysfunction in the central nervous system. In this review, we underlined that FIR requires modulations of janus kinase 2 / signal transducer and activator of transcription 3 (JAK2/STAT3), nuclear factor E2-related factor 2 (Nrf-2), muscarinic M1 acetylcholine receptor (M1 mAChR), dopamine D1 receptor, protein kinase C δ gene, and glutathione peroxidase-1 gene for exerting the protective potentials in response to neuropsychotoxic conditions.

KEYWORDS:

Dopamine D1 receptor; Far-infrared ray; Glutathione peroxidase-1; JAK2/STAT3; M1 mAChR; Neuropsychotoxic conditions; Nuclear factor E2-related factor 2; Protein kinase C δ gene

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