Atrial fibrillation (AF) is the most common type of cardiac arrhythmia and increases the risk for stroke, heart failure and death. However, current antiarrhythmic therapy has moderate efficacy and considerable risks. Thus, there is a need for effective and safe therapeutic drugs for AF. The atrial inflammatory response, oxidative stress and fibrosis are common pathological alterations in AF. 1 Increasing evidence indicates that inflammation and its related immune response play a crucial role in the initiation and maintenance of AF. 1,2 Indeed, clinical studies have indicated that the recruitment of immune cells such as monocytes and macrophages and the levels of pro-inflammatory cytokines, such as C-reactive protein (CRP), tumour necrosis factor (TNF)-α, interleukin (IL)-2, IL-6, IL-8 and monocyte