Hsin-Hung Chen1,2, Tung-Chen Yeh3, Pei-Wen Cheng1,2,4, Wen-Yu Ho5,6, Chiu-Yi Ho1,7, Chi-Cheng Lai8, Gwo-Ching Sun9,10, Ching-Jiunn Tseng1,7,11,12. 1. Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, 81362, Taiwan. 2. Yuh-Ing Junior College of Health Care & Management, Kaohsiung, 80776, Taiwan. 3. Cardiovascular Center, Kaohsiung Veterans General Hospital, Kaohsiung, 81362, Taiwan. 4. Department of Physical Therapy, Shu-Zen Junior College of Medicine and Management, Kaohsiung, 82144, Taiwan. 5. Division of General Internal Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan. 6. Division of Internal Medicine, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan. 7. Institute of Biomedical Sciences, National Sun Yat-sen University, Kaohsiung, 80424, Taiwan. 8. Cardiology, Kaohsiung Municipal United Hospital, Kaohsiung, 80457, Taiwan. 9. Department of Anesthesiology, Kaohsiung Medical University Hospital, Kaohsiung, 80708, Taiwan. 10. Department of Anesthesiology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan. 11. Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, 40447, Taiwan. 12. Department of Pharmacology, National Defense Medical Center, Taipei, 11490, Taiwan.
Abstract
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.
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 hypertensiverats. 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.