Artemisinin suppresses sympathetic hyperinnervation following myocardial infarction via anti-inflammatory effects.

Inflammation plays an important role in sympathetic remodeling after myocardial infarction (MI), and the inhibition of inflammation has therapeutic benefits that could alleviate the progression of sympathetic remodeling. Recent studies have indicated that the antimalarial agent artemisinin has the ability to inhibit inflammation. In this study, the inhibitory effects of artemisinin on the production of proinflammatory mediators and the number of macrophages were investigated 4 weeks after MI. Our results show that artemisinin significantly inhibited IL-1β and TNF-α protein expression and the infiltration of macrophages. Artemisinin significantly decreased the protein expression of NGF, GAP43, and TH compared with the control group, which was related to sympathetic nerve remodeling. Interestingly, a clear positive correlation was observed between the expression of NGF and GAP43 in our study, and a similar correlation was revealed between NGF and TH. In addition, the densities of both GAP-43- and TH-immunoreactive nerves in the peri-infarct zone were significantly attenuated by artemisinin treatment. Our results suggest that artemisinin is able to inhibit sympathetic remodeling after MI, possibly through an anti-inflammatory effect. The data provide direct evidence of the potential application of artemisinin for the treatment of sympathetic remodeling after MI.