Sesamin suppresses angiotensin‐II‐enhanced oxidative stress and hypertrophic markers in H9c2 cells

Author:

Chang Chih‐Chia12,Cheng Hui‐Ching3,Chou Wan‐Ching3,Huang Yu‐Ting4,Hsieh Pei‐Ling5,Chu Pei‐Ming67,Lee Shin‐Da89ORCID

Affiliation:

1. Department of Radiation Therapy and Oncology Ditmanson Medical Foundation Chia‐Yi Christian Hospital Chia‐Yi Taiwan

2. Department of Medical Laboratory and Biotechnology Asia University Taichung Taiwan

3. Department of Orthopedic Surgery E‐Da Hospital/I‐Shou University Kaohsiung Taiwan

4. Institute of Allied Health Sciences, College of Medicine National Cheng Kung University Tainan Taiwan

5. Department of Anatomy, School of Medicine China Medical University Taichung Taiwan

6. Department of Anatomy, School of Medicine Chung Shan Medical University Taichung Taiwan

7. Department of Medical Education Chung Shan Medical University Hospital Taichung Taiwan

8. Department of Physical Therapy, Graduate Institute of Rehabilitation Science China Medical University Taichung Taiwan

9. Department of Physical Therapy Asia University Taichung Taiwan

Abstract

AbstractMyocardial hypertrophy plays a crucial role in cardiovascular disease (CVD) development. Myocardial hypertrophy is an adaptive response by myocardial cells to stress after cardiac injury to maintain cardiac output and function. Angiotensin II (Ang‐II) regulates CVD through the renin‐angiotensin‐aldosterone system, and its signaling in cardiac myocytes leads to excessive reactive oxygen species (ROS) production, oxidative stress, and inflammation. Sesamin (SA), a natural compound in sesame seeds, has anti‐inflammatory and anti‐apoptotic effects. This study investigated whether SA could attenuate hypertrophic damage and oxidative injuries in H9c2 cells under Ang‐II stimulation. We found that SA decreased the cell surface area. Furthermore, Ang‐II treatment reduced Ang‐II‐increased ANP, BNP, and β‐MHC expression. Ang‐II enhanced NADPH oxidase activity, ROS formation, and decreased Superoxide Dismutase (SOD) activity. SA treatment reduces Ang‐II‐caused oxidative injuries. We also found that SA mitigates Ang‐II‐induced apoptosis and pro‐inflammatory responses. In conclusion, SA could attenuate Ang‐II‐induced cardiac hypertrophic injuries by inhibiting oxidative stress, apoptosis, and inflammation in H9c2 cells. Therefore, SA might be a potential supplement for CVD management.

Funder

China Medical University

Asia University

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Management, Monitoring, Policy and Law,Toxicology,General Medicine

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