Neohesperidin inhibits cardiac remodeling induced by Ang II in vivo and in vitro

• Published in: Biomedicine & pharmacotherapy 2020-09, Vol.129, p.110364-110364, Article 110364
• Main Authors: Zhang, Jingsi, Fu, Xiaodan, Yang, Li, Wen, Hongxin, Zhang, Lijiao, Liu, Fengyi, Lou, Yu, Yang, Qian, Ding, Yanchun
• Format: Article
• Language: English
• Subjects: Angiotensin II; Animals; Cardiac remodeling; Cells, Cultured; Disease Models, Animal; Fibrosis; Gene Expression Regulation; Hesperidin - analogs & derivatives; Hesperidin - pharmacology; Hypertrophy; Hypertrophy, Left Ventricular - metabolism; Hypertrophy, Left Ventricular - pathology; Hypertrophy, Left Ventricular - physiopathology; Hypertrophy, Left Ventricular - prevention & control; Inflammation Mediators - metabolism; Male; Mice, Inbred C57BL; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; Neohesperidin; Oxidative stress; Oxidative Stress - drug effects; Rats, Sprague-Dawley; Signal Transduction; Ventricular Function, Left - drug effects; Ventricular Remodeling - drug effects
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2020.110364

[Display omitted] •Neohesperidin inhibits cardiac fibrosis induced by Ang II in mice.•Neohesperidin inhibits cardiac hypertrophy induced by Ang II in mice.•Neohesperidin reduce cardiac remodeling induced by Ang II. Cardiac hypertrophy and remodeling are among the major health challenges facing countries around the world today. Neohesperidin plays an important role in influencing cell apoptosis, cell growth, tumorigenesis and tumor microenvironment, but the mechanism and role of Neohesperidin in cardiac hypertrophy and remodeling caused by Angiotensin II has not been fully elucidated. This study used Angiotensin II to induce cardiac hypertrophy and cardiac remodeling in mice. Echocardiography was used to evaluate cardiac function, H&E and Masson trichrome staining were used to detect myocardial histological changes. Cardiac cell size was determined by WGA staining. The protein content of the signaling pathway was detected by Western blot, and the mRNA expression of fibrosis and hypertrophy markers was detected by qPCR. DHE staining was used to detect oxidative stress. We also observed the effect of Neohesperidin on Ang II-induced NRCMs. The results showed that neohesperidin can significantly inhibit Ang II-induced myocardial contractile dysfunction, cardiac hypertrophy, myocardial fibrosis, myocardial oxidative stress and inflammation. These results suggest that Neohesperidin can alleviate cardiac hypertrophy and remodeling caused by Ang II, and its mechanism may be related to the inhibition of multiple signaling pathways.