Aging
Navigate
Submit an Article
Research Paper|Volume 14, Issue 16|pp 6740—6755

Sulforaphane inhibits angiotensin II-induced cardiomyocyte apoptosis by acetylation modification of Nrf2

Huanhuan Wang1,2,3, Ge Yang4, Yuan Tian4, Jinjie Li4, Lingbin Meng5, Xin Jiang1,2,3, Ying Xin4
  • 1Jilin Provincial Key Laboratory of Radiation Oncology and Therapy, The First Hospital of Jilin University, Changchun 130021, Jilin, China
  • 2Department of Radiation Oncology, The First Hospital of Jilin University, Changchun 130021, Jilin, China
  • 3NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun 130021, Jilin, China
  • 4Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun 130021, Jilin, China
  • 5Department of Hematology and Medical Oncology, Moffitt Cancer Center, Tampa, FL 33612, USA
Received: March 29, 2022Accepted: August 15, 2022Published: August 23, 2022
https://doi.org/10.18632/aging.204247

Copyright: © 2022 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Oxidative stress is the central cause of angiotensin II (Ang II)-induced myocardial injury, and nuclear factor erythroid 2-related factor (Nrf2) is the core molecule of the anti-oxidant defense system. We have previously demonstrated that sulforaphane (SFN) can prevent Ang II-induced myocardial injury by activating Nrf2; however, the underlying molecular mechanism is still unclear. This study aimed to evaluate whether SFN prevents Ang II-induced cardiomyocyte apoptosis through acetylation modification of Nrf2. Wild-type and Nrf2 knockdown embryonic rat cardiomyocytes (H9C2) were exposed to Ang II to induce apoptosis, oxidative stress, and inflammatory responses. SFN treatment significantly reduced Ang II-induced cardiomyocyte apoptosis, inflammation and oxidative stress. Activation of Nrf2 played a critical role in preventing cardiomyocyte apoptosis. After Nrf2 was knockdown, the anti-inflammatory, antioxidant stress of SFN were eliminated. Furthermore, Nrf2 activation by SFN was closely related to the decreased activity of histone deacetylases (HDACs) and increased histone-3 (H3) acetylation levels in Nrf2 promoter region. These findings confirm that Nrf2 plays a key role in SFN preventing Ang II-induced cardiomyocyte apoptosis. SFN activates Nrf2 by inhibiting HDACs expression and activation.