Aim To explore the effects and mechanisms of transplantation of macrophages transfected with heme oxygenase-1 (HO-1) gene by adenovirus vectors on inflammation, oxidative stress in acute myocardial infarction (AMI) area. Methods Rat alveolar macrophages were cultured in vitro and divided into three groups and treated differently:control group, the cells were not transfected with adenovirus; Ad-Mφ group, the cells were transfected with blank adenovirus vector; Ad-HO-1-Mφ group, the cells were transfected with adenovirus carrying the HO-1 gene. The proliferative activity of macrophages and the expression of HO-1 protein as well as the inflammatory cytokines such as tumor necrosis factor (TNF-α), interleukelin-6 (IL-6), IL-10 in the supernatant were detected. In addition, The AMI model in rats were established by ligating coronary artery and randomly divided into three groups:the simple AMI group, the Ad-Mφ transplantation group and the Ad-HO-1-Mφ transplantation group. PBS, PBS containing 2×10⁵ Ad-Mφ and PBS containing 2×10⁵ Ad-HO-1-Mφ were injected into the myocardial infarction area of rats in each group respectively. 5 days later, the expression of HO-1 protein and the inflammatory cytokines such as IL-12, TNF-α, IL-10, monocyte chemotactic protein 1 (MCP-1) as well as the total antioxidant capacity (T-AOC) and malondialdehyde (MDA) content in infarcted myocardium were detected. Results Adenovirus transfection itself did not affect macrophage proliferation activity, but could transfer HO-1 gene into macrophage and obtain high expression. Ad-HO-1-Mφ could significantly reduce the expression of pro-inflammatory cytokine TNF-α, IL-6 and increase the expression of anti-inflammatory factor IL-10 (P<0.05). Compared with the simple AMI group and the Ad-Mφ transplantation group, the infarcted area of Ad-HO-1-Mφ transplantation group showed much more expression of HO-1 protein and IL-10 and less expression of TNF-α, IL-12, MCP-1 while T-AOC increased and MDA content decreased significantly (P<0.05 respectively). Conclusion Ad-HO-1-Mφ could overexpress HO-1 protein and polarize into M2 phenotype which has powerful anti-inflammatory properties. After being transplanted into myocardial infarcted area, the Ad-HO-1-Mφ could still overexpress HO-1 protein and significantly reduce the inflammation and oxidative stress levels in myocardial infracted area.