The data showed that the TUNEL-positive cells, Caspase3 and Bax protein expressions in the heart tissues of sepsis mice increased, and Bcl2 was significantly downregulated (p < 0.05 vs. sham group, Figures 1J–L), whereas Deh treatment markedly decreased TUNEL-labeled cardiomyocytes, inhibited Bax and Caspase3 expression, and promoted Bcl2 level in a dose-dependent manner (p < 0.05 vs. sepsis group Figures 1J–L). This evidence concerns the gene BCL2 and Sepsis.