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Antioxidants
Volume 11
Issue 9
10.3390/antiox11091745
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Article

NADPH Oxidase Mediates Oxidative Stress and Ventricular Remodeling through SIRT3/FOXO3a Pathway in Diabetic Mice

by
Jiuchun Qiu
1,†,
Daiqi Liu
1,†,
Pengsha Li
1,
Lingling Zhou
1,2,
Lu Zhou
1,
Xing Liu
1,
Yue Zhang
1,
Meng Yuan
1,
Gary Tse
1,
Guangping Li
1 and
Tong Liu
1,*
1
Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin 300211, China
2
Department of Cardiology, Wenzhou People’s Hospital, No. 299 Guan Road, Wenzhou 325000, China
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Antioxidants 2022, 11(9), 1745; https://doi.org/10.3390/antiox11091745
Submission received: 28 July 2022 / Revised: 29 August 2022 / Accepted: 30 August 2022 / Published: 2 September 2022
(This article belongs to the Special Issue Oxidative Balance and Heart Function: A Physiological Lifelong Challenge)
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Abstract

Oxidative stress and mitochondrial dysfunction are important mechanisms of ventricular remodeling, predisposed to the development of diabetic cardiomyopathy (DCM) in type 2 diabetes mellitus. In this study, we have successfully established a model of type 2 diabetes using a high-fat diet (HFD) in combination with streptozotocin (STZ). The mice were divided into three groups of six at random: control, diabetes, and diabetes with apocynin and the H9c2 cell line was used as an in vitro model for investigation. We examined the molecular mechanisms of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation on mitochondrial dysfunction and ventricular remodeling in the diabetic mouse model. Hyperglycemia-induced oxidative stress led to a reduced expression of sirtuin 3 (SIRT3), thereby promoting forkhead box class O 3a (FOXO3a) acetylation in ventricular tissue and H9c2 cells. Reactive oxygen species (ROS) overproduction promoted ventricular structural modeling and conduction defects. These alterations were mitigated by inhibiting NADPH oxidase with the pharmaceutical drug apocynin (APO). Apocynin improved SIRT3 and Mn-SOD expression in H9c2 cells transfected with SIRT3 siRNA. In our diabetic mouse model, apocynin improved myocardial mitochondrial function and ROS overproduction through the recovery of the SIRT3/FOXO3a pathway, thereby reducing ventricular remodeling and the incidence of DCM.
Keywords: NADPH oxidase; oxidative stress; diabetic cardiomyopathy NADPH oxidase; oxidative stress; diabetic cardiomyopathy

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MDPI and ACS Style

Qiu, J.; Liu, D.; Li, P.; Zhou, L.; Zhou, L.; Liu, X.; Zhang, Y.; Yuan, M.; Tse, G.; Li, G.; et al. NADPH Oxidase Mediates Oxidative Stress and Ventricular Remodeling through SIRT3/FOXO3a Pathway in Diabetic Mice. Antioxidants 2022, 11, 1745. https://doi.org/10.3390/antiox11091745

AMA Style

Qiu J, Liu D, Li P, Zhou L, Zhou L, Liu X, Zhang Y, Yuan M, Tse G, Li G, et al. NADPH Oxidase Mediates Oxidative Stress and Ventricular Remodeling through SIRT3/FOXO3a Pathway in Diabetic Mice. Antioxidants. 2022; 11(9):1745. https://doi.org/10.3390/antiox11091745

Chicago/Turabian Style

Qiu, Jiuchun, Daiqi Liu, Pengsha Li, Lingling Zhou, Lu Zhou, Xing Liu, Yue Zhang, Meng Yuan, Gary Tse, Guangping Li, and et al. 2022. "NADPH Oxidase Mediates Oxidative Stress and Ventricular Remodeling through SIRT3/FOXO3a Pathway in Diabetic Mice" Antioxidants 11, no. 9: 1745. https://doi.org/10.3390/antiox11091745

APA Style

Qiu, J., Liu, D., Li, P., Zhou, L., Zhou, L., Liu, X., Zhang, Y., Yuan, M., Tse, G., Li, G., & Liu, T. (2022). NADPH Oxidase Mediates Oxidative Stress and Ventricular Remodeling through SIRT3/FOXO3a Pathway in Diabetic Mice. Antioxidants, 11(9), 1745. https://doi.org/10.3390/antiox11091745

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