Assessment of Liver Damage in an Experimental Model of Streptozotocin-Induced Diabetes in Sprague Dawley Rats: Focusing on Morphological and Oxidative Stress Status

Abstract

Objective: Diabetes mellitus (DM) is a widespread metabolic disorder that causes severe complications, including damage to various organs. The liver, a pivotal organ involved in metabolic regulation, is particularly vulnerable to diabetic injury. This study aimed to investigate the effects of diabetes on the liver, using streptozotocin (STZ)-induced diabetic model in Sprague Dawley rats. Methods: Twelve male rats were divided into control and diabetic groups. Diabetes was induced via intraperitoneal injection of a single dose of STZ (55 mg/kg), and after eight weeks, the rats were sacrificed, and the liver tissues were collected for analysis of histological changes, apoptosis, and oxidative stress markers. Results: Histological evaluations demonstrated significant alterations in diabetic liver tissue, characterized by hepatocyte degeneration, fibrosis, and cellular swelling. Immunohistochemical analysis revealed elevated active caspase-3 expression, indicating increased apoptosis in diabetic livers. Additionally, the analysis of oxidative stress markers revealed a significant increase in H2O2 levels, while superoxide dismutase activity remained unchanged, suggesting an oxidative imbalance. Conclusion: These findings confirm that diabetes leads to liver damage through mechanisms including apoptosis, fibrosis, and oxidative stress, emphasizing the significance of therapeutic approaches targeting these pathways. In this respect, future research should focus on these mechanisms in other DM models and include additional liver injury biomarkers to better understand the progression of diabetic liver disease.