Abstract
Empagliflozin is a selective sodium-glucose cotransporter-2 (SGLT2) inhibitor widely used in the management of type 2 diabetes (T2DM). In addition to its glucose-lowering activity, empagliflozin possess anti-inflammatory and metabolic regulatory properties. Diabetes is a chronic metabolic disorder characterized by persistent hyperglycemia and is frequently associated with structural and functional alterations in multiple organs, including the liver. This study evaluated the histopathological effects of empagliflozin on hepatic tissue in an alloxan-induced diabetic rat model. Fifteen adult male rats were randomly assigned into three groups (n = 5 per group): a healthy control group, an untreated diabetic group, and a diabetic group treated with empagliflozin (5 mg/kg/day) for 30 days. Diabetes was induced using alloxan monohydrate, and liver tissue was subsequently collected for histopathological examination using hematoxylin and eosin staining.
Microscopic examination revealed severe hepatic alterations in untreated diabetic rats, including hepatocellular necrosis, central vein congestion, sinusoidal dilatation, hemorrhage, nuclear degeneration, and disruption of normal hepatic architecture. In the empagliflozin-treated group, partial preservation of liver structure was observed; however, several pathological features persisted, including inflammatory cell infiltration, sinusoidal hemorrhage, hepatocellular hypertrophy, nuclear pyknosis, and early hepatic steatosis. Although empagliflozin treatment appeared to attenuate some histopathological abnormalities, complete restoration of normal liver structure was not achieved within the experimental period. The findings suggest that the observed hepatic injury was primarily associated with alloxan-induced toxicity and diabetes-related pathologic processes. Under the conditions of this study, empagliflozin exhibited limited hepatoprotective activity despite modest preservation of hepatic architecture. Further studies involving larger sample sizes, extended treatment durations, and molecular investigations are required to clarify the
Microscopic examination revealed severe hepatic alterations in untreated diabetic rats, including hepatocellular necrosis, central vein congestion, sinusoidal dilatation, hemorrhage, nuclear degeneration, and disruption of normal hepatic architecture. In the empagliflozin-treated group, partial preservation of liver structure was observed; however, several pathological features persisted, including inflammatory cell infiltration, sinusoidal hemorrhage, hepatocellular hypertrophy, nuclear pyknosis, and early hepatic steatosis. Although empagliflozin treatment appeared to attenuate some histopathological abnormalities, complete restoration of normal liver structure was not achieved within the experimental period. The findings suggest that the observed hepatic injury was primarily associated with alloxan-induced toxicity and diabetes-related pathologic processes. Under the conditions of this study, empagliflozin exhibited limited hepatoprotective activity despite modest preservation of hepatic architecture. Further studies involving larger sample sizes, extended treatment durations, and molecular investigations are required to clarify the
Keywords
Empagliflozin