The Effect of Aminoguanidine on Fibrinogen Gene Expression and Oxidative Stress Biomarkers in the Liver Tissue of a Streptozotocin-Induced Diabetic Rat Model.

OBJECTIVES

Oxidative stress promotes the initiation and progression of diabetic complications. Fibrinogen is a thrombotic factor proposed as a biomarker for prognostic assessment, as a marker for tracking vascular complications, and as a therapeutic target in diabetes. Aminoguanidine, an inhibitor of advanced glycation end products and inducible nitric oxide synthase, has been shown to reduce oxidative stress and related vascular injury. However, the underlying processes still need to be entirely elucidated. This study investigated the effects of aminoguanidine on oxidative stress biomarkers and fibrinogen gene expression in diabetic rats.

MATERIALS AND

METHODS

Twenty-four male rats, matched for body weight and age, were randomly assigned to five groups: (intended n = 6 per group). Due to mortality during the study, the final group sizes were: healthy controls (n = 5), untreated diabetic controls (n = 4), and diabetic rats treated with aminoguanidine at 50, 100, or 200 mg/kg (n = 6, 4, and 5, respectively). Diabetes mellitus was induced by intraperitoneal injection of streptozotocin (50 mg/kg) in rats fasted for 12 h. One week later, diabetic rats received aminoguanidine for 28 days. The liver was selected for analysis due to its key role in oxidative stress and metabolism. Malondialdehyde (MDA) and ferric-reducing ability of plasma (FRAP) were measured in liver tissue as markers of oxidative stress, and fibrinogen gene expression was assessed by real-time polymerase chain reaction.

RESULTS

Aminoguanidine at 50 mg/kg significantly reduced fibrinogen gene expression (p = 0.047). Hepatic MDA levels decreased at all doses (50, 100, and 200 mg/kg, p < 0.05), while FRAP levels increased significantly at 50 and 100 mg/kg (p < 0.05).

CONCLUSION

Aminoguanidine may attenuate oxidative stress and fibrinogen gene expression in the livers of diabetic rats.