Atorvastatin alleviates renal ischemia-reperfusion injury in rats by promoting M1-M2 transition

Acute kidney injury (AKI) often occurs as a result of ischemia-reperfusion (IR). Previous studies have demonstrated that inflammation is an important contributor to AKI. Atorvastatin (ATO) possesses anti‑inflammatory properties and has been demonstrated to exert protective effects against renal IR injury (IRI). However, the underlying mechanism requires further study. In the present study, a rat model of renal IRI was successfully established. Consistent with the results of a previous study, ATO significantly attenuated IRI, which was supported by a decrease in serum creatinine and an increase in creatinine clearance rate, as well as alleviated pathological alterations in renal tubular cells. There are two types of activated macrophages: Proinflammatory M1 and anti‑inflammatory M2 macrophages, which have been demonstrated to exert contributory and protective effects on IRI, respectively. The present study demonstrated that treatment with ATO significantly decreased M1 macrophage density and increased M2 macrophage density, as compared with the IR group. In addition, it is well known that M1 macrophages can be induced by T helper 1 cytokines, including tumor necrosis factor (TNF)‑α and interferon (IFN)‑γ, whereas M2 macrophages can be induced by peroxisome proliferator-activated receptor (PPAR)‑γ. The present study indicated that ATO treatment significantly decreased the expression levels of TNF‑α and IFN‑γ, and increased PPAR‑γ expression. In conclusion, ATO may ameliorate renal IRI by promoting M1‑M2 transition. Furthermore, ATO‑mediated macrophage polarization in rats with renal IRI may be associated with the downregulation of TNF‑α and IFN‑γ, and the upregulation of PPAR-γ.