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Oral CoQ10 attenuates high salt-induced hypertension by restoring neurotransmitters and cytokines in the hypothalamic paraventricular nucleus.
Sci Rep 2016; 6:30301SR

Abstract

High salt intake leads to an increase in some proinflammatory cytokines and neurotransmitters involved in the pathogenesis of hypertension. The purpose of this work was to know if oral administration of anti-oxidant and free-radical scavenger CoQ10 may attenuate high salt-induced hypertension via regulating neurotransmitters and cytokines in the hypothalamic paraventricular nucleus (PVN). Adult male Sprague-Dawley (SD) rats were fed with a normal salt diet (NS, 0.3% NaCl) or a high salt diet (HS, 8% NaCl) for 15 weeks to induce hypertension. These rats received CoQ10 (10 mg/kg/day) dissolved in olive oil was given by gavage (10 mg/kg/day) for 15 weeks. HS resulted in higher mean arterial pressure (MAP) and the sympathetic nerve activity (RSNA). These HS rats had higher PVN levels of norepinephrine (NE), tyrosine hydroxylase (TH), interleukin (IL)-1β, NOX2 and NOX4, lower PVN levels of gamma-aminobutyric acid (GABA), IL-10, copper/zinc superoxide dismutase (Cu/Zn-SOD) and the 67-kDa isoform of glutamate decarboxylase (GAD67), as compared with NS group. CoQ10 supplementation reduced NE, TH, IL-1β, NOX2 and NOX4 in the PVN, and induced IL-10, Cu/Zn-SOD and GAD67 in the PVN. These findings suggest that CoQ10 supplementation restores neurotransmitters and cytokines in the PVN, thereby attenuating high salt-induced hypertension.

Authors+Show Affiliations

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Pharmaceutical Analysis, School of Pharmacy, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Endocrinology and Metabolism, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Cardiology, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an 710061, China.Department of Cardiology, First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an 710061, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Physiology, Nanjing Medical University, Nanjing 210029, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China. Department of Pharmacology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Cardiovascular Research Center, Xi'an Jiaotong University Health Science Center, Xi'an 710061, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27452860

Citation

Gao, Hong-Li, et al. "Oral CoQ10 Attenuates High Salt-induced Hypertension By Restoring Neurotransmitters and Cytokines in the Hypothalamic Paraventricular Nucleus." Scientific Reports, vol. 6, 2016, p. 30301.
Gao HL, Yu XJ, Qi J, et al. Oral CoQ10 attenuates high salt-induced hypertension by restoring neurotransmitters and cytokines in the hypothalamic paraventricular nucleus. Sci Rep. 2016;6:30301.
Gao, H. L., Yu, X. J., Qi, J., Yi, Q. Y., Jing, W. H., Sun, W. Y., ... Kang, Y. M. (2016). Oral CoQ10 attenuates high salt-induced hypertension by restoring neurotransmitters and cytokines in the hypothalamic paraventricular nucleus. Scientific Reports, 6, p. 30301. doi:10.1038/srep30301.
Gao HL, et al. Oral CoQ10 Attenuates High Salt-induced Hypertension By Restoring Neurotransmitters and Cytokines in the Hypothalamic Paraventricular Nucleus. Sci Rep. 2016 07 25;6:30301. PubMed PMID: 27452860.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oral CoQ10 attenuates high salt-induced hypertension by restoring neurotransmitters and cytokines in the hypothalamic paraventricular nucleus. AU - Gao,Hong-Li, AU - Yu,Xiao-Jing, AU - Qi,Jie, AU - Yi,Qiu-Yue, AU - Jing,Wang-Hui, AU - Sun,Wen-Yan, AU - Cui,Wei, AU - Mu,Jian-Jun, AU - Yuan,Zu-Yi, AU - Zhao,Xiu-Fang, AU - Liu,Kai-Li, AU - Zhu,Guo-Qing, AU - Shi,Xiao-Lian, AU - Liu,Jin-Jun, AU - Kang,Yu-Ming, Y1 - 2016/07/25/ PY - 2016/01/25/received PY - 2016/07/04/accepted PY - 2016/7/26/entrez PY - 2016/7/28/pubmed PY - 2018/4/24/medline SP - 30301 EP - 30301 JF - Scientific reports JO - Sci Rep VL - 6 N2 - High salt intake leads to an increase in some proinflammatory cytokines and neurotransmitters involved in the pathogenesis of hypertension. The purpose of this work was to know if oral administration of anti-oxidant and free-radical scavenger CoQ10 may attenuate high salt-induced hypertension via regulating neurotransmitters and cytokines in the hypothalamic paraventricular nucleus (PVN). Adult male Sprague-Dawley (SD) rats were fed with a normal salt diet (NS, 0.3% NaCl) or a high salt diet (HS, 8% NaCl) for 15 weeks to induce hypertension. These rats received CoQ10 (10 mg/kg/day) dissolved in olive oil was given by gavage (10 mg/kg/day) for 15 weeks. HS resulted in higher mean arterial pressure (MAP) and the sympathetic nerve activity (RSNA). These HS rats had higher PVN levels of norepinephrine (NE), tyrosine hydroxylase (TH), interleukin (IL)-1β, NOX2 and NOX4, lower PVN levels of gamma-aminobutyric acid (GABA), IL-10, copper/zinc superoxide dismutase (Cu/Zn-SOD) and the 67-kDa isoform of glutamate decarboxylase (GAD67), as compared with NS group. CoQ10 supplementation reduced NE, TH, IL-1β, NOX2 and NOX4 in the PVN, and induced IL-10, Cu/Zn-SOD and GAD67 in the PVN. These findings suggest that CoQ10 supplementation restores neurotransmitters and cytokines in the PVN, thereby attenuating high salt-induced hypertension. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/27452860/Oral_CoQ10_attenuates_high_salt_induced_hypertension_by_restoring_neurotransmitters_and_cytokines_in_the_hypothalamic_paraventricular_nucleus_ L2 - http://dx.doi.org/10.1038/srep30301 DB - PRIME DP - Unbound Medicine ER -