17βH-Neriifolin from Cerbera odollam Gaertn. prevents angiotensin II-induced cardiomyocyte hypertrophy in H9c2 cells

 which progresses from cardiac remodeling. It is a condition that is manifested by the cardiac enlargement or clinically known as cardiac hypertrophy which reduces cardiac functions. 17βH-Neriifolin (1) is a cardiac glycoside isolated from Cerbera odollam Gaertn leaves. To determine the effects of 17βH-neriifolin on angiotensin II (Ang II)-induced cardiomyocyte hypertrophy in H9c2 cardiomyocytes. The cardiomyocytes were concurrently exposed to Ang II (500 nM) in the absence or presence of 17βH-neriifolin (3 µM) or digoxin (5 µM) for 24 h. Digoxin served as the positive control, while a group without any treatment was the control. Ang II significantly increased cell surface area, which was prevented by 17βH-neriifolin and digoxin. Ang II also augmented reactive oxygen species and nitric oxide cellular levels, nuclear factor-kB (NF-kB), inducible nitric oxide synthase and sodium-potassium ATPase (Na+/K+-ATPase) protein expressions and activities. Both 17βH-neriifolin and digoxin inhibited these Ang II-induced changes. The effects afforded by 17βH-neriifolin were similar to that of digoxin. 17βH-neriifolin showed cardioprotective effects against Ang II-induced detrimental effects in H9c2 cells, possibly by reducing Na+/K+-ATPase, iNOS, NF-kB expressions, and intracellular ROS as well as restoring nitric oxide levels.