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. The gene discussed is HIF1A; the disease is cardiac hypertrophy.