Leonurine protects cardiac function following acute myocardial infarction through anti‑apoptosis by the PI3K/AKT/GSK3β signaling pathway.

Abstract

Leonurine is a compound derived from Herba leonuri, which has been reported to protect cardiac tissue against ischemic injury via antioxidant and anti-apoptosis effects. The present study investigated whether these effects may be applied to acute myocardial infarction (MI) and examined the underlying mechanisms of leonurine treatment. A rat model of MI was induced by coronary artery ligation. Leonurine was administered at 15 mg/kg/day by oral gavage following the onset of MI. Rats in the sham group and the saline group were administered with an equal volume of saline. Echocardiography, Masson's trichrome staining, and terminal-deoxynucleotidyl transferase-mediated dUTP nick end labeling assays were performed 28 days post MI. The expression of B-cell lymphoma-2 and Bax were assessed by western blot analysis and reverse transcription-quantitative polymerase chain reaction. Phosphoinositide 3-kinase (PI3K), protein kinase B and glycogen synthase kinase-3β (GSK3β) protein expression were investigated by western blot analysis. Leonurine significantly alleviated collagen deposition and MI size, inhibited cell apoptosis and improved myocardial function. This was accompanied by significantly increased levels of phosphorylated (p)-PI3K, p-AKT, p-GSK3β and Bcl-2, as well as significantly decreased levels of caspase3, cleaved-caspase3 and Bax following MI. The results demonstrated that leonurine exerts potent cardio-protective effects in a rat model of MI by inducing anti-apoptotic effects by activating the PI3K/AKT/GSK3β signaling pathway.