Ursolic Acid Mitigates Cardiac Dysfunction in Mice with Lipopolysaccharide-induced Sepsis

This study aimed to investigate the protective effect of ursolic acid (UA) on cardiac dysfunction in mice with lipopolysaccharide (LPS)-induced sepsis and the mechanism. Forty-two mice were randomly divided into control, model and UA groups, 14 mice in each group. The LPS-induced sepsis model was established in model and UA groups. In UA group, the UA was intraperitoneally injected (10 mL/kg) for six days, and then LPS was injected intraperitoneally on the 7th day. After 6 h from intraperitoneal injection of LPS, the hemodynamics, serum indicators, myocardial inflammatory factors and oxidative stress indexes, and myocardial apoptosis protein expressions were determined. Results showed that, compared with model group, in UA group the LVSP, LVEDP, +dp/dt(max) and -dp/dt(max) were increased, the serum cardiac troponin I and brain natriuretic peptid levels were decreased, the myocardial tumor necrosis factor alpha, interleukin 1 beta, reactive oxygen species and malondialdehyde levels were decreased, the myocardial superoxide dismutase and glutathione peroxidase levels were increased, the myocardial B-cell lymphoma-2 protein level was increased, and the B-cell lymphoma-2 associated X protein level was decreased. In conclusion, the UA pretreatment can mitigate the cardiac dysfunction in mice with LPS-induced sepsis by reducing inflammatory response and oxidative stress in myocardial tissue and inhibiting cardiomyocyte apoptosis.