Abstract
Far-infrared ray (FIR) therapy has been reported to exert beneficial effects on cardiovascular function by elevating endothelial nitric oxide synthesis (eNOS) activity and nitric oxide (NO) production. Tetrahydrobiopterin (BH4) is a key determinant of eNOS-dependent NO synthesis in vascular endothelial cells. However, whether BH4 synthesis is associated with the effects of FIR on eNOS/NO production has not yet been investigated. In this study, we investigated the effects of FIR on BH4-dependent eNOS/NO production and vascular function. We used FIR-emitting sericite boards as an experimental material and placed human umbilical vein endothelial cells (HUVECs) and Sprague–Dawley rats on the boards with or without FIR irradiation and then evaluated vascular relaxation by detecting NO generation, BH4 synthesis, and Akt/eNOS activation. Our results showed that FIR radiation significantly enhanced Akt/eNOS phosphorylation and NO production in human endothelial cells and aorta tissues. FIR can also induce BH4 storage by elevating levels of enzymes (e.g., guanosine triphosphate cyclohydrolase-1, 6-pyruvoyl tetrahydrobiopterin synthase, sepiapterin reductase, and dihydrofolate reductase), which ultimately results in NO production. These results indicate that FIR upregulated eNOS-dependent NO generation via BH4 synthesis and Akt phosphorylation, which contributes to the regulation of vascular function. This might develop potential clinical application of FIR to treat vascular diseases by augmenting the BH4/NO pathway.
Highlights
Vascular endothelial cells, which are located in the inner surfaces of blood vessels, have a pivotal role in modulating vascular tone and blood fluidity through the release of vasoactive substances [1]. e endothelial isoform of nitric oxide synthase is robustly expressed in endothelial cells, and is a main source of vascular nitric oxide (NO), a major endothelium-dependent relaxing factor [2]
We investigated the whether BH4 synthesis and Akt phosphorylation are associated with the effects of FIRemitting sericite boards on vasodilation via endothelial isoform of nitric oxide synthase (eNOS)/NO production
Compared to Far-infrared ray (FIR) devices and saunas, FIRemitting materials are more applied for different medical conditions [20, 21]. e FIR-emitting sericite boards used in this study were made from sericite nanoparticles, which could be incorporated into fibers and woven into fabrics for textile manufacture
Summary
Vascular endothelial cells, which are located in the inner surfaces of blood vessels, have a pivotal role in modulating vascular tone and blood fluidity through the release of vasoactive substances [1]. e endothelial isoform of nitric oxide synthase (eNOS) is robustly expressed in endothelial cells, and is a main source of vascular nitric oxide (NO), a major endothelium-dependent relaxing factor [2]. [3] evidence has shown that Akt, a downstream target of phosphatidylinositol 3-kinase (PI3K), activates eNOS phosphorylation in endothelial cells [5]. Erefore, both the PI3K/Akt pathway and BH4 synthesis play a role in regulating blood vessel vasodilatation via eNOS/NO production. Emerging studies have indicated that FIR therapy improves the health of patients with cardiovascular diseases, diabetes, inflammation, and other diseases [8,9,10,11]. These studies revealed only that FIR therapy has a protective effect on impaired vascular diseases; the underlying molecular mechanisms of the effects of FIR on eNOS/NO production have not been investigated. We investigated the whether BH4 synthesis and Akt phosphorylation are associated with the effects of FIRemitting sericite boards on vasodilation via eNOS/NO production
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