Furthermore, the STAT3 specific inhibitor S3I‐201 or the depletion of STAT3 expression by siRNA could alleviate AngII‐induced cardiac hypertrophy in H9c2 cells following PM treatment, while PM failed to reduce the expressions of hypertrophy‐related proteins (Collagen I, α‐SMA, TGF‐β1 and ANP) and phosphorylated STAT3 in STAT3‐overexpressing cells, suggesting that PM‐mediated protection against AngII‐induced cardiac hypertrophy depended on modulation of the STAT3 signalling axis. This evidence concerns the gene ACTA1 and cardiac hypertrophy.