He et al. (2017) showed that HPS upregulated PPAR by reducing blood glucose and lipid-γ levels. The progression of DCM can be delayed by increasing GLUT-4 expression. HPS has been shown to mitigate the apoptosis of human umbilical vein endothelial cells (HUVEC) caused by high glucose levels, according to Liu et al. (2012). Dong (2018) found that in the DCM model, HPS treatment increased B-cell lymphoma/leukemia-2 (Bcl-2) expression in db/db mouse myocardium tissue while decreasing caspase-3 and Bax expression. The gene discussed is SLC2A4; the disease is familial dilated cardiomyopathy.