Background <p>Renal ischemia-reperfusion (IR) injury is a leading cause of acute kidney injury and a major obstacle in renal transplantation. Oxidative stress (OS), inflammation, and apoptosis contribute to tissue damage. Carvacrol (CAR), a natural monoterpenic phenol, exhibits antioxidant and anti-apoptotic properties, yet its dual protective and therapeutic potential in renal IR injury has not been fully clarified. To evaluate the protective and therapeutic effects of CAR on renal function, OS, histopathology, and apoptosis in a rat model of renal IR injury.</p> Methods <p>Thirty-two female Wistar albino rats were randomly allocated to four groups (<i>n</i> = 8): Control, IR, CAR + IR (pre-ischemic CAR), and IR + CAR (post-ischemic CAR). All underwent right nephrectomy and left renal ischemia (60&#xa0;min) followed by reperfusion (24&#xa0;h). CAR (73&#xa0;mg/kg, intraperitoneal) was administered 30&#xa0;min before ischemia or immediately after reperfusion. Serum renal function markers (blood urea nitrogen, creatinine, albumin), renal OS parameters [malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH)], histopathological changes, and caspase-3 immunoreactivity were assessed.</p> Results <p>IR caused significant increases in blood urea nitrogen, creatinine, MDA, and caspase-3 expression, along with reductions in albumin, SOD, and CAT (<i>p</i> &lt; 0.05). Both pre- and post-ischemic CAR administration significantly improved renal function, restored antioxidant enzyme activity, reduced MDA levels, and ameliorated histopathological damage (<i>p</i> &lt; 0.05). Pre-ischemic CAR additionally suppressed caspase-3 immunoreactivity, indicating a stronger anti-apoptotic effect.</p> Conclusion <p>CAR confers renoprotective benefits in renal IR injury through antioxidant and anti-apoptotic mechanisms. Its efficacy in both preventive and therapeutic settings underscores its translational potential for clinical use in renal surgery and transplantation.</p>