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Sesamin suppresses angiotensin‐II‐enhanced oxidative stress and hypertrophic markers in H9c2 cells
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 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.
Sesamin suppresses angiotensin‐II‐enhanced oxidative stress and hypertrophic markers in H9c2 cells
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 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.
Sesamin suppresses angiotensin‐II‐enhanced oxidative stress and hypertrophic markers in H9c2 cells
Chang, Chih‐Chia (author) / Cheng, Hui‐Ching (author) / Chou, Wan‐Ching (author) / Huang, Yu‐Ting (author) / Hsieh, Pei‐Ling (author) / Chu, Pei‐Ming (author) / Lee, Shin‐Da (author)
Environmental Toxicology ; 38 ; 2165-2172
2023-09-01
8 pages
Article (Journal)
Electronic Resource
English
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