Aim To investigate the effects of ginsenoside Rg1 on arrhythmia after myocardial ischemia reperfusion (I/R) in rats based on peroxisome proliferator-activated receptor-γ(PPAR-γ). Methods 72 SD rats were randomly divided into sham-operated group (SO group), ischemia-reperfusion group (I/R group), ginsenoside Rg1 group (Rg1 group), ginsenoside Rg1 + rosiglitazone group (Rg1 + ROS group). The left anterior descending coronary artery was ligated in the last three groups to establish I/R model. The SO group and I/R group were given saline intervention, the Rg1 group was given 40 mg/kg ginsenoside Rg1 intervention, and the Rg1 + ROS group was given 40 mg/kg ginsenoside Rg1 + 6 mg/kg ROS intervention. ECG was monitored during 6 hours of reperfusion. Myocardial I/R area, myocardial enzymes, inflammatory cytokines and expressions of nuclear factor-κB (NF-κB), inhibitor of NF-κBand PPAR-γ were detected after 6 hours of reperfusion. Results Compared with SO group, arrhythmia in I/R group significantly aggravated, myocardial I/R area, the contents of creatine phosphate kinase (CK), creatine phosphate kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), P-selectin, E-selectin and the expression of NF-κB, PPAR-γ significantly increased, while the expression of I-κB expression significantly decreased. Compared with I/R group, arrhythmia in Rg1 group significantly improved, the contents of myocardial I/R area, CK, CK-MB, LDH, TNF-α, IL-1β, P-selectin, E-selectin and the expression of NF-κB, PPAR-γ significantly decreased, while the expression of I-κB expression significantly increased; Compared with Rg1 group, the arrhythmia of Rg1+ROS group significantly aggravated, the contents of myocardial I/R area, CK, CK-MB, LDH, TNF-α, IL-1β, P-selectin, E-selectin and the expression of NF-κB, PPAR-γ significantly increased, while the expression of I-κB expression significantly decreased. Conclusion Ginsenoside Rg1 can improve myocardial arrhythmia after I/R by inhibiting PPAR-γ-mediated inflammation.