Artemisinin prevents electric remodeling following myocardial infarction possibly by upregulating the expression of connexin 43.

Artemisinin has been demonstrated to exert beneficial effects on ventricular remodeling. The present study investigated whether artemisinin was able to decrease the ventricular fibrillation threshold (VFT) in rats following myocardial infarction (MI) and aimed to determine the possible underlying mechanisms. The rats were subjected to surgery to induce MI by ligation of the left anterior descending artery and were randomly allocated to receive vehicle or artemisinin (75 mg/kg/day) treatment for four weeks. Programmed electrical stimulation demonstrated a significantly increased VFT in the artemisinin-treated group compared with the vehicle-treated group. The electrophysiological improvement of the VFT was accompanied by increased immunofluorescence-stained connexin 43 (Cx43), myocardial Cx43 protein and mRNA levels in artemisinin-treated rats. The present study also demonstrated that artemisinin significantly decreased tissue tumor necrosis factor (TNF)-α levels at the infarcted border zone. Thus, artemisinin demonstrated a protective effect on ventricular arrhythmias following MI. Although the precise mechanism by which artemisinin modulates the dephosphorylation of Cx43 is unknown, it is likely that artemisinin increased the expression of Cx43 via the inhibition of TNF-α.