Pogostone alleviates angiotensin II-induced cardiomyocyte hypertrophy in H9c2 cells through MAPK and Nrf2 pathway

Purpose: To investigate the effect of pogostone on cardiac hypertrophy.Methods: An in vitro model of myocardial hypertrophy was first established by stimulating H9c2 (rat cardiomyocytes) with angiotensin II (Ang II), and the cells treated with or without pogostone. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were measured by western blot. Immunofluorescence staining was performed for α-actinin while cell surface area was quantified. Dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe and malondialdehyde (MDA) assay kit were used to determine reactive oxygen species (ROS) and MDA levels respectively. Apoptosis was evaluated by flow cytometry while Nrf2, p38, ERK, and JNK protein expression levels were determined by western-blot assay.Results: Compared with the control group, ANP and BNP protein expression levels, cell surface area, ROS, MDA, and apoptosis were all elevated in H9c2 cells after stimulation with Ang II (p < 0.001). Varying doses of pogostone decreased protein expressions of ANP and BNP, reduced cell surface area, decreased ROS and MDA levels, and inhibited apoptosis. Pogostone also up-regulated and inhibited the phosphorylation levels of p38 and ERK, and JNK levels in H9c2 cells.Conclusion: Pogostone reduces protein expression of ANP and BNP and up-regulated Nrf2 protein expression in H9c2 cells stimulated with angiotensin II.