| In recent years, liver transplantation has emerged as the standard therapy for several liver disorders. Throughout the procedure, the transplanted liver tissue is subjected to varying degrees of ischemia-reperfusion damage. Consequently, there has been a long-standing pursuit of substances that can alleviate the harm caused by ischemia-reperfusion. In our investigation, we employed dapagliflozin as a potential therapeutic agent. Eighteen Wistar rats were divided into three groups (n = 6) including treatment, ischemia-reperfusion (IR), and control that did not undergo surgical intervention. Two days prior to surgery, the treatment group received dapagliflozin at a dosage of 10 mg kg-1 PO. During surgery, liver ischemia was induced for one hour, followed by a 24-hr reperfusion period. The IR group exhibited elevated levels of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP), bilirubin, lactate dehydrogenase (LDH), and malondialdehyde (MDA) compared to the control group. In contrast, the treatment group showed levels of these factors that were closer to those of the control group. While total protein, albumin, and total antioxidant capacity decreased in the IR group, this decline was less significant in the treatment group. Analysis of oxidative stress in liver tissue revealed that the treatment group had increased antioxidant capacity and exhibited less oxidative stress compared to the IR group. Furthermore, dapagliflozin was found to reduce the degree of liver edema, necrosis, and vascular hyperemia following ischemia-reperfusion. Overall, dapagliflozin demonstrates the potential to lessen liver damage, enhance liver tissue regeneration, and mitigate the consequences associated with liver impairment. |