PM effectively reduced myocardial hypertrophy caused by AngII and TAC, manifested by decreased cell surface area and reduced expressions of hypertrophy‐related markers (Collagen I, α‐SMA, TGF‐β1 and ANP), implying that PM is a bioactive compound that improves myocardial hypertrophy and is worth further exploration. The gene discussed is ACTA1; the disease is cardiac hypertrophy.