Pathological
cardiac hypertrophy is characterized by an abnormal increase in cardiac muscle mass in the left ventricle, resulting in cardiac dysfunction. Although various therapeutic approaches are being continuously developed for
heart failure, several studies have suggested natural compounds as novel potential strategies. Considering relevant compounds, we investigated a new role for
Pterosin B for which the potential life-affecting biological and
therapeutic effects on cardiomyocyte
hypertrophy are not fully known. Thus, we investigated whether
Pterosin B can regulate cardiomyocyte
hypertrophy induced by
angiotensin II (Ang II) using H9c2 cells. The antihypertrophic effect of
Pterosin B was evaluated, and the results showed that it reduced
hypertrophy-related gene expression, cell size, and
protein synthesis. In addition, upon Ang II stimulation,
Pterosin B attenuated the activation and expression of major receptors, Ang II type 1 receptor and a
receptor for advanced glycation end products, by inhibiting the phosphorylation of PKC-ERK-NF-κB pathway signaling molecules. In addition,
Pterosin B showed the ability to reduce excessive intracellular
reactive oxygen species, critical mediators for
cardiac hypertrophy upon Ang II exposure, by regulating the expression levels of
NAD(P)H oxidase 2/4. Our results demonstrate the protective role of
Pterosin B in cardiomyocyte
hypertrophy, suggesting it is a potential therapeutic candidate.