This study aimed to establish a dexamethasone model as a representative model for metabolic-associated hepatic injury in male Wistar rats. dexamethasone is a synthetic glucocorticoid with potent anti-inflammatory effects and high glucocorticoid activity. The model was developed to induce insulin resistance and nonalcoholic fatty liver disease in a relatively short period.
Male Wistar rats were allotted into three groups: control, DEX8, and DEX16. The rats of DEX8 and DEX16 groups were injected intraperitoneally with dexamethasone for 6 days at doses of 8 mg/kg/day and 16 mg/kg/day, respectively. Fasting blood glucose levels were measured, and various biochemical parameters were analyzed. Liver sections were collected and examined for histopathological changes.
The results showed that dexamethasone administration significantly increased fasting blood glucose levels compared to the control group. Liver indices were also significantly elevated in the dexamethasone-administered groups. Moreover, serum alanine aminotransferase and aspartate aminotransferase activities were significantly increased in the dexamethasone groups, indicating liver damage. Histopathological examination revealed hydropic degeneration, portal edema, leukocyte infiltration, and fibrosis in the liver sections of dexamethasone-treated rats.
These findings demonstrate that the dexamethasone model successfully induced metabolic-associated hepatic injury in male Wistar rats, as evidenced by hyperglycemia, altered liver indices, increased liver enzymes, and histopathological changes resembling NASH. The model provides a valuable tool for studying the pathophysiology of metabolic liver diseases and evaluating potential therapeutic interventions. It offers a convenient and time-efficient approach to investigate the effects of dexamethasone and develop strategies to mitigate its adverse effects on liver function.