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Antihypertensive Potential of Coenzyme Q10 via Free Radical Scavenging and Enhanced Akt‐nNOS Signaling in the Nucleus Tractus Solitarii in Rats
Author(s) -
Chen HsinHung,
Yeh TungChen,
Cheng PeiWen,
Ho WenYu,
Ho ChiuYi,
Lai ChiCheng,
Sun GwoChing,
Tseng ChingJiunn
Publication year - 2019
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201801042
Subject(s) - coenzyme q10 , chemistry , nadph oxidase , protein kinase b , reactive oxygen species , medicine , endocrinology , apocynin , nicotinamide adenine dinucleotide phosphate , superoxide dismutase , superoxide , fructose , oxidase test , pharmacology , biochemistry , oxidative stress , phosphorylation , enzyme
Scope In the Natural Medicines database, coenzyme Q10 (CoQ10) is classified as possibly effective for the treatment of hypertension. Patients with hypertension frequently have a significant deficiency of the antioxidant CoQ10. Furthermore, reactive oxygen species are overproduced in the nucleus tractus solitarii (NTS) during the cardiovascular regulation of hypertension in vivo. However, the molecular mechanisms by which CoQ10 modulates cardiovascular functions in the NTS are unclear. In this study, the effects of CoQ10 on superoxide generation, downstream NO signaling in the NTS, and blood pressure were evaluated in rats with fructose‐induced hypertension. Methods and Results Treatment with oral CoQ10 for 4 weeks abolished nicotinamide adenine dinucleotide phosphate‐oxidase (NADPH oxidase) activation, decreased p38 phosphorylation, and increased superoxide dismutase 2 production in the NTS of fructose‐fed rats. The serum levels of uric acid decrease in response to CoQ10 treatment in fructose‐fed rats. Oral CoQ10 reduced blood pressure by inducing Akt and nNOS phosphorylation in NTS of fructose‐induced hypertensive rats. Conclusion Oral CoQ10 decreases blood pressure by negatively regulating fructose‐induced NADPH oxidase levels, abolishing ROS generation, reducing p38 phosphorylation, and enhancing the Akt‐nNOS pathway in the NTS. These results support the beneficial effects of CoQ10 in oxidative stressassociated hypertension.