Tags

Type your tag names separated by a space and hit enter

Tert-butylhydroquinone attenuates oxidative stress and inflammation in hypothalamic paraventricular nucleus in high salt-induced hypertension.
Toxicol Lett 2017; 281:1-9TL

Abstract

Excessive oxidative stress and inflammation in hypothalamic paraventricular nucleus (PVN) are implicated in the pathogenesis of hypertension. It is reported that tert-butylhydroquinone (tBHQ), a nuclear factor erythroid 2-related factor 2(Nrf2)-inducer, has a variety of pharmacological activities such as anti-oxidation and anti-inflammatory effect. The objective of this study was to investigate the effects of tBHQ in high salt induced hypertension and to identify whether the beneficial effects were induced by inhibiting PVN oxidative stress and inflammation. Male Sprague-Dawley rats were fed with high salt diet (HS, 8% NaCl) or normal salt diet (NS, 0.3% NaCl). These rats were administration of tBHQ (150mg/kg/d) by oral gavage for 16 weeks. Our results showed that high salt intake resulted in higher mean arterial pressure, cardiac hypertrophy as well as increased plasma level of norepinephrine and interleukin (IL)-1β, IL-6 compared with NS rats. It increased PVN level of reactive oxygen species, gp91phox, IL-1β, IL-6, p-IKKβ and nuclear factor-kappa B (NF-κB) activity, decreased PVN level of Nrf2 and Cu/Zn-SOD. Chronic administration of tBHQ significantly attenuated these changes in HS rats. These data suggest that the protective effects of tBHQ in salt induced hypertension are partly due to inhibiting oxidative stress and inflammation in PVN.

Authors+Show Affiliations

Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China. Electronic address: yuxiaojing@mail.xjtu.edu.cn.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, 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, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China.Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, Nanjing, 210029, China.Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.Department of Endocrinology and Metabolism, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, China.Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Basic Medical Sciences, Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an 710061, China. Electronic address: ykang@mail.xjtu.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28844481

Citation

Bai, Juan, et al. "Tert-butylhydroquinone Attenuates Oxidative Stress and Inflammation in Hypothalamic Paraventricular Nucleus in High Salt-induced Hypertension." Toxicology Letters, vol. 281, 2017, pp. 1-9.
Bai J, Yu XJ, Liu KL, et al. Tert-butylhydroquinone attenuates oxidative stress and inflammation in hypothalamic paraventricular nucleus in high salt-induced hypertension. Toxicol Lett. 2017;281:1-9.
Bai, J., Yu, X. J., Liu, K. L., Wang, F. F., Li, H. B., Shi, X. L., ... Kang, Y. M. (2017). Tert-butylhydroquinone attenuates oxidative stress and inflammation in hypothalamic paraventricular nucleus in high salt-induced hypertension. Toxicology Letters, 281, pp. 1-9. doi:10.1016/j.toxlet.2017.08.018.
Bai J, et al. Tert-butylhydroquinone Attenuates Oxidative Stress and Inflammation in Hypothalamic Paraventricular Nucleus in High Salt-induced Hypertension. Toxicol Lett. 2017 Nov 5;281:1-9. PubMed PMID: 28844481.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tert-butylhydroquinone attenuates oxidative stress and inflammation in hypothalamic paraventricular nucleus in high salt-induced hypertension. AU - Bai,Juan, AU - Yu,Xiao-Jing, AU - Liu,Kai-Li, AU - Wang,Fang-Fang, AU - Li,Hong-Bao, AU - Shi,Xiao-Lian, AU - Zhang,Yan, AU - Huo,Chan-Juan, AU - Li,Xiang, AU - Gao,Hong-Li, AU - Qi,Jie, AU - Liu,Jin-Jun, AU - Zhu,Guo-Qing, AU - Chen,Wen-Sheng, AU - Cui,Wei, AU - Kang,Yu-Ming, Y1 - 2017/08/24/ PY - 2017/06/02/received PY - 2017/08/18/revised PY - 2017/08/20/accepted PY - 2017/8/29/pubmed PY - 2017/11/7/medline PY - 2017/8/29/entrez KW - Hypertension KW - Hypothalamic paraventricular nucleus KW - Inflammation KW - Oxidative stress KW - Tert-butylhydroquinone SP - 1 EP - 9 JF - Toxicology letters JO - Toxicol. Lett. VL - 281 N2 - Excessive oxidative stress and inflammation in hypothalamic paraventricular nucleus (PVN) are implicated in the pathogenesis of hypertension. It is reported that tert-butylhydroquinone (tBHQ), a nuclear factor erythroid 2-related factor 2(Nrf2)-inducer, has a variety of pharmacological activities such as anti-oxidation and anti-inflammatory effect. The objective of this study was to investigate the effects of tBHQ in high salt induced hypertension and to identify whether the beneficial effects were induced by inhibiting PVN oxidative stress and inflammation. Male Sprague-Dawley rats were fed with high salt diet (HS, 8% NaCl) or normal salt diet (NS, 0.3% NaCl). These rats were administration of tBHQ (150mg/kg/d) by oral gavage for 16 weeks. Our results showed that high salt intake resulted in higher mean arterial pressure, cardiac hypertrophy as well as increased plasma level of norepinephrine and interleukin (IL)-1β, IL-6 compared with NS rats. It increased PVN level of reactive oxygen species, gp91phox, IL-1β, IL-6, p-IKKβ and nuclear factor-kappa B (NF-κB) activity, decreased PVN level of Nrf2 and Cu/Zn-SOD. Chronic administration of tBHQ significantly attenuated these changes in HS rats. These data suggest that the protective effects of tBHQ in salt induced hypertension are partly due to inhibiting oxidative stress and inflammation in PVN. SN - 1879-3169 UR - https://www.unboundmedicine.com/medline/citation/28844481/Tert_butylhydroquinone_attenuates_oxidative_stress_and_inflammation_in_hypothalamic_paraventricular_nucleus_in_high_salt_induced_hypertension_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-4274(17)31265-1 DB - PRIME DP - Unbound Medicine ER -