Although treatment of rats with 2 ME further decreased the AAC-mediated inhibition of phosphorylated p38, 2 ME significantly normalized the AAC-mediated effect on the phosphorylated ERK1/2 indicating a crucial role of the MAPK signaling pathway in the protective effect of 2 ME against AAC induced left ventricular hypertrophy (Fig. 4). This evidence concerns the gene MAPK3 and left ventricular hypertrophy.