To determine the mechanism by which MA suppressed the inflammation and apoptosis in MI/RI, we analyzed the effects of MA on the signaling pathways involving HMGB1, a vital mediator in the pathophysiology of the MI/RI through TLR4-MyD88-NF-κB mediated signaling, and may represent an important therapeutic target (12, 15). Here, TLR4 is linked to myocardial infarction.