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

被引:7
作者
Chang, Chih-Chia [1 ,2 ]
Cheng, Hui-Ching [3 ]
Chou, Wan-Ching [3 ]
Huang, Yu-Ting [4 ]
Hsieh, Pei-Ling [5 ]
Chu, Pei-Ming [6 ,7 ]
Lee, Shin-Da [8 ,9 ,10 ]
机构
[1] Chia Yi Christian Hosp, Ditmanson Med Fdn, Dept Radiat Therapy & Oncol, Chiayi, Taiwan
[2] Asia Univ, Dept Med Lab & Biotechnol, Taichung, Taiwan
[3] I Shou Univ, E Da Hosp, Dept Orthoped Surg, Kaohsiung, Taiwan
[4] Natl Cheng Kung Univ, Inst Allied Hlth Sci, Coll Med, Tainan, Taiwan
[5] China Med Univ, Sch Med, Dept Anat, Taichung, Taiwan
[6] Chung Shan Med Univ, Sch Med, Dept Anat, Taichung, Taiwan
[7] Chung Shan Med Univ Hosp, Dept Med Educ, Taichung, Taiwan
[8] China Med Univ, Grad Inst Rehabil Sci, Dept Phys Therapy, Taichung, Taiwan
[9] Asia Univ, Dept Phys Therapy, Taichung, Taiwan
[10] China Med Univ, Dept Phys Therapy, Taichung, Taiwan
关键词
angiotensin-II; apoptosis; inflammation; myocardial hypertrophy; sesamin; INDUCED CARDIAC-HYPERTROPHY; APOPTOSIS; PROTECTS;
D O I
10.1002/tox.23853
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Myocardial 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 & beta;-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.
引用
收藏
页码:2165 / 2172
页数:8
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