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Far-Infrared-Emitting Sericite Board Upregulates Endothelial Nitric Oxide Synthase Activity through Increasing Biosynthesis of Tetrahydrobiopterin in Endothelial Cells

机译:远红外发射绢云母板通过增加内皮细胞中四氢螺旋蛋白的生物合成来提高内皮一氧化氮合成酶活性

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摘要

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.
机译:据报道,目前红外线(FIR)治疗通过升高内皮一氧化氮合成(ENOS)活性和一氧化氮(NO)生产来对心血管功能产生有益效果。四氢螺旋素(BH4)是血管内皮细胞中依赖于烯醇的关键决定簇。但是,BH4合成是否与FIR对ENOS的影响/没有生产尚未进行调查。在这项研究中,我们研究了FIR对BH4依赖性ENOS / NO生产和血管功能的影响。我们使用杉木发射绢云母板作为实验材料,并将人脐静脉内皮细胞(HUVECS)和Sprague-Dawley大鼠在有或没有冷冻辐射的情况下,然后通过检测不代的BH4合成和AKT / enos激活。我们的研究结果表明,FIR辐射显着增强了AKT / enos磷酸化,在人类内皮细胞和主动脉组织中没有生产。冷杉还可以通过升高酶水平(例如,鸟苷三磷酸环氢化酶-1,6-丙酮氟四氢替替素合酶,Sepiapterin还原酶和二氢氢醇还原酶)来诱导BH4储存,最终导致没有生产。这些结果表明,FIR上调通过BH4合成和Akt磷酸化的依赖性不产生,这有助于调节血管功能。这可能会通过增强BH4 / No途径来发展杉木治疗血管疾病的潜在临床应用。

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