Beta3-Adrenergic Receptor Activation Alleviates Cardiac Dysfunction in Cardiac Hypertrophy by Regulating Oxidative Stress

Author:

Zhang Mingming1ORCID,Xu Yuerong2,Chen Jianghong1,Qin Chaoshi1,Liu Jing1,Guo Dong1,Wang Rui1,Hu Jianqiang1,Zou Qing1,Yang Jingxiao1,Wang Zikuan1,Niu Xiaolin1ORCID

Affiliation:

1. Department of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi’an, China

2. Department of Orthodontics, School of Stomatology, The Fourth Military Medical University, Xi’an, China

Abstract

Background. Excessive myocardial oxidative stress could lead to the congestive heart failure. NADPH oxidase is involved in the pathological process of left ventricular (LV) remodeling and dysfunction. β3-Adrenergic receptor (AR) could regulate cardiac dysfunction proved by recent researches. The molecular mechanism of β3-AR regulating oxidative stress, especially NADPH oxidase, remains to be determined. Methods. Cardiac hypertrophy was constructed by the transverse aortic constriction (TAC) model. ROS and NADPH oxidase subunits expression were assessed after β3-AR agonist (BRL) or inhibitor (SR) administration in cardiac hypertrophy. Moreover, the cardiac function, fibrosis, heart size, oxidative stress, and cardiomyocytes apoptosis were also detected. Results. β3-AR activation significantly alleviated cardiac hypertrophy and remodeling in pressure-overloaded mice. β3-AR stimulation also improved heart function and reduced cardiomyocytes apoptosis, oxidative stress, and fibrosis. Meanwhile, β3-AR stimulation inhibited superoxide anion production and decreased NADPH oxidase activity. Furthermore, BRL treatment increased the neuronal NOS (nNOS) expression in cardiac hypertrophy. Conclusion. β3-AR stimulation alleviated cardiac dysfunction and reduced cardiomyocytes apoptosis, oxidative stress, and fibrosis by inhibiting NADPH oxidases. In addition, the protective effect of β3-AR is largely attributed to nNOS activation in cardiac hypertrophy.

Funder

Shaanxi Province Science and Technology New Star Project

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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