Study of peroxisome proliferator–activated receptor (PPAR)-γ in renal ischemia–reperfusion injury

Abstract Recent studies of ischemia–reperfusion (I/R) injury have focused on the function of neutrophils, the action mechanism of inflammatory cytokines. However, few reports have addressed peroxisome proliferator–activated receptor (PPAR)-γ. PPAR-γ is a ligand-activated transcriptional factor belonging to the steroid receptor superfamily. It plays a role in both adipocyte differentiation and tumorigenesis. We researched the expression of PPAR-γ in renal I/R injury of the rat. Male Lewis rats were used. The right kidney was harvested and the left renal artery and vein were clamped at 90 minutes of ischemic time. Rats were killed at 0, 1.5, 3, 5, and 12 hours after reperfusion. PPAR-γ expression was studied by immunohistostaining. PPAR-γ expression was observed only on mesangial and endothelial cells of normal kidney. From 1.5 to 3 hours after reperfusion, PPAR-γ expression gradually became stronger on mesangial and endothelial cells. PPAR-γ expression was most intense on mesangial cells and endothelial cells at 3 hours after reperfusion. Twelve hours after reperfusion, necrosis extended throughout the ischemic kidney and nearly all the tubular epithelial cells were destroyed, but 12 hours after reperfusion PPAR-γ expression gradually became weaker on mesangial and endothelial cells. PPAR-γ was expressed in the rat model having renal I/R injury. Several hours after maximal of PPAR-γ expression, maximal renal I/R injury was observed. These results may indicate a relationship between PPAR-γ expression and renal I/R injury.