Ischemia‑reperfusion (I/R) injury is important in the pathogenesis and/or progression of various diseases, including stroke, cardiovascular disease and acute renal injury. Increasing evidence indicates that atorvastatin exerts protective effects in I/R injury‑associated diseases; however, the underlying mechanisms remain to be fully elucidated. In the present study, oxygen‑glucose deprivation (OGD)/reperfusion‑stimulated. RAW264.7 murine macrophages served as a model of I/R injury. The knockdown of peroxisome proliferator activated receptor‑γ (PPARγ) expression in these cells increased OGD/reperfusion‑induced expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor‑α (TNF‑α) and interferon‑γ (IFN‑γ), and enhanced OGD/reperfusion‑induced downregulation of the expression of cluster of differentiation (CD) 206, at the mRNA and protein levels. Conversely, overexpression of PPARγ significantly attenuated OGD/reperfusion‑induced alterations in the expression of iNOS, TNF‑α, IFN‑γ and CD206 at the mRNA and protein levels. Notably, atorvastatin inhibited OGD/reperfusion‑induced iNOS expression and reversed OGD/reperfusion‑induced downregulation of the expression of CD206 and PPARγ at the mRNA and protein levels. The results of the present study indicate that atorvastatin exhibits significant anti‑inflammatory effects in OGD/reperfusion‑stimulated RAW264.7 cells, possibly via PPARγ regulation. The findings of the present study may reveal a novel mechanism underlying the protective effects of atorvastatin in I/R injury‑associated diseases.