scholarly journals Far-infrared Ray-mediated Antioxidant Potentials are Important for Attenuating Psychotoxic Disorders

2019 ◽  
Vol 17 (10) ◽  
pp. 990-1002 ◽  
Author(s):  
Naveen Sharma ◽  
Eun-Joo Shin ◽  
Nam Hun Kim ◽  
Eun-Hee Cho ◽  
Bao Trong Nguyen ◽  
...  
Keyword(s):  
Far Infrared ◽  
D1 Receptor ◽  
Janus Kinase ◽  
Receptor Protein ◽  
Related Factor ◽  
Memory Impairments ◽  
Glutathione Peroxidase 1 ◽  
The Central Nervous System ◽  
Far Infrared Ray ◽  
Transcription 3

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 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.

Analyses on the Manufacture and Physical Properties of Electromagnetic Shielding/ Far Infrared Ray Nonwoven

2010 ◽  
Vol 97-101 ◽  
pp. 1790-1793
Author(s):  
Jia Horng Lin ◽  
Yu Tien Huang ◽  
Chin Mei Lin ◽  
Yi Chang Yang ◽  
Chien Teng Hsieh ◽  
...  
Keyword(s):  
Physical Properties ◽  
Far Infrared ◽  
Electromagnetic Shielding ◽  
Breaking Force ◽  
Shielding Effectiveness ◽  
Machine Direction ◽  
Tear Strength ◽  
Burst Strength ◽  
Far Infrared Ray ◽  
Electromagnetic Shielding Effectiveness

According to the results, when low melting polyester fiber increased to be 20%, the electromagnetic shielding/ far infrared ray nonwoven obtained the optimum burst strength, maximum breaking force and maximum tear strength, and they were as follows: burst strength was 4.2 kgf/cm2; maximum breaking force was 153.59 N in the cross machine direction and 70.80 N in the machine direction; maximum tear strength was 215.77 N in cross machine direction and 117.07 N in machine direction; and optimum electromagnetic shielding effectiveness (EMSE) was 45 dB.

Effects of far infrared ray (FIR) on human hepatoma cell HepG2

2009 ◽  
Author(s):  
Tatsuo Ishikawa ◽  
Kikuji Yamashita ◽  
Jun Ishibashi ◽  
Kaori Sumida ◽  
Takahumi Masui ◽  
...  
Keyword(s):  
Hepatoma Cell ◽  
Far Infrared ◽  
Human Hepatoma ◽  
Human Hepatoma Cell ◽  
Far Infrared Ray ◽  
Cell Hepg2

scholarly journals Myeloid-derived cullin 3 promotes STAT3 phosphorylation by inhibiting OGT expression and protects against intestinal inflammation

2017 ◽  
Vol 214 (4) ◽  
pp. 1093-1109 ◽  
Author(s):  
Xinghui Li ◽  
Zhibin Zhang ◽  
Lupeng Li ◽  
Wei Gong ◽  
Audrey J. Lazenby ◽  
...  
Keyword(s):  
Ubiquitin Ligase ◽  
Posttranslational Modification ◽  
Intestinal Inflammation ◽  
Inhibitory Effect ◽  
Related Factor ◽  
Colonic Inflammation ◽  
Stat3 Phosphorylation ◽  
Cullin 3 ◽  
Glcnac Transferase ◽  
Transcription 3

Signal transducer and activator of transcription 3 (STAT3) is a key mediator of intestinal inflammation and tumorigenesis. However, the molecular mechanism that modulates STAT3 phosphorylation and activation is not fully understood. Here, we demonstrate that modification of STAT3 with O-linked β-N-acetylglucosamine (O-GlcNAc) on threonine 717 (T717) negatively regulates its phosphorylation and targets gene expression in macrophages. We further found that cullin 3 (CUL3), a cullin family E3 ubiquitin ligase, down-regulates the expression of the O-GlcNAc transferase (OGT) and inhibits STAT3 O-GlcNAcylation. The inhibitory effect of CUL3 on OGT expression is dependent on nuclear factor E2–related factor-2 (Nrf2), which binds to the Ogt promoter region and increases gene transcription. Myeloid deletion of Cul3 led to defective STAT3 phosphorylation in colon macrophages, which was accompanied by exacerbated colonic inflammation and inflammation-driven tumorigenesis. Thus, this study identifies a new form of posttranslational modification of STAT3, modulating its phosphorylation, and suggests the importance of immunometabolism on colonic inflammation and tumorigenesis.

scholarly journals Ezetimibe Attenuates Oxidative Stress and Neuroinflammation via the AMPK/Nrf2/TXNIP Pathway after MCAO in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Jing Yu ◽  
Wen-na Wang ◽  
Nathanael Matei ◽  
Xue Li ◽  
Jin-wei Pang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Brain Infarction ◽  
Neutrophil Infiltration ◽  
Artery Occlusion ◽  
Receptor Protein ◽  
Related Factor ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Interacting Protein

Oxidative stress and neuroinflammation play essential roles in ischemic stroke-induced brain injury. Previous studies have reported that Ezetimibe (Eze) exerts antioxidative stress and anti-inflammatory properties in hepatocytes. In the present study, we investigated the effects of Eze on oxidative stress and neuroinflammation in a rat middle cerebral artery occlusion (MCAO) model. One hundred and ninety-eight male Sprague-Dawley rats were used. Animals assigned to MCAO were given either Eze or its control. To explore the downstream signaling of Eze, the following interventions were given: AMPK inhibitor dorsomorphin and nuclear factor erythroid 2-related factor 2 (Nrf2) siRNA. Intranasal administration of Eze, 1 h post-MCAO, further increased the endogenous p-AMPK expression, reducing brain infarction, neurologic deficits, neutrophil infiltration, microglia/macrophage activation, number of dihydroethidium- (DHE-) positive cells, and malonaldehyde (MDA) levels. Specifically, treatment with Eze increased the expression of p-AMPK, Nrf2, and HO-1; Romo-1, thioredoxin-interacting protein (TXNIP), NOD-like receptor protein 3 (NLRP3), Cleaved Caspase-1, and IL-1β were reduced. Dorsomorphin and Nrf2 siRNA reversed the protective effects of Eze. In summary, Eze decreases oxidative stress and subsequent neuroinflammation via activation of the AMPK/Nrf2/TXNIP pathway after MCAO in rats. Therefore, Eze may be a potential therapeutic approach for ischemic stroke patients.

scholarly journals Zisheng Shenqi Decoction Ameliorates Monosodium Urate-Mediated Gouty Arthritis in Rats via Promotion of Autophagy through the AMPK/mTOR Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jieru Han ◽  
Guangyu Shi ◽  
Wenhao Li ◽  
Shuhui Wang ◽  
Jixiang Bai ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Gouty Arthritis ◽  
Nitrogen Monoxide ◽  
Joint Space ◽  
Mtor Signaling ◽  
Receptor Protein ◽  
Related Factor ◽  
Monosodium Urate ◽  
Mtor Signaling Pathway

Gouty arthritis (GA) is an inflammatory disease owing to the accumulation of monosodium urate (MSU) in joints, leading to redness and burning pain. In this study, the effect of Zisheng Shenqi Decoction (ZSD) on a rat model of MSU-induced GA was investigated. ZSD obviously diminished the right paw thickness, the degree of the swelling of the paw, and the infiltration of the inflammatory cell, as well as cartilage erosion, and widened the joint space in MSU-treated rats. Besides, MSU remarkably elevated the release of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-18; however, ZSD treatment dose dependently lowered these levels and resulted in a significant decrease in articular elastase activity. Also, ZSD administration increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) but declined malondialdehyde (MDA) and nitrogen monoxide (NO) contents. Importantly, western blotting analysis revealed that NOD-like receptor protein 3 (NLRP3), cleaved caspase-1, IL-1β, nuclear factor-E2-related factor 2 (Nrf2) in the cytoplasm, phosphorylated mammalian target of rapamyclin (p-mTOR), and p62 expressions were downregulated, whereas the levels of nuclear Nrf2, phosphorylated AMP-activated protein kinase (p-AMPK), Beclin-1, and LC3II/I were upregulated by ZSD. Immunofluorescence assay indicated that ZSD evidently promoted nuclear translocation of LC3. Taken together, ZSD inhibited inflammation and oxidative stress and facilitated autophagy through the activation of the AMPK pathway and suppression of the mTOR signaling pathway, demonstrating its potential for preventing and curing GA.

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