Overall, our animal studies showed that by activating the p38 MAPK signaling pathway, BPS inhibited the production of inflammatory factors caused by oxidative stress in type-2 DM, decreased the protein levels of HIF-1α, TNF-α, and MMP-9 in myocardial tissues, downregulated caspase-3 levels, and increased the ratio of Bcl-2/Bax, thus decreasing inflammatory injury, reducing myocardial apoptosis, improving myocardial ischemia and myocardial hypertrophy, delaying heart failure, and delaying the progression of DCM. This evidence concerns the gene BAX and cardiac hypertrophy.