Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia, which can lead to various complications, including damage to the pancreas and kidney. This study investigates the efficacy of sericin (Ser) treatment in mitigating fibrosis and related complications in streptozotocin (STZ)-induced diabetic rats. Diabetes induction led to increased serum glucose, HbA1c, oxidative stress markers (H₂O₂, AGEs), and pro-inflammatory mediators (NF-κB, TNFα, INF-γ, TGF-β), along with reduced antioxidant defenses, including total antioxidant capacity (TAC) and pancreatic glutathione reductase (GR) activity. Digestive enzyme activities (amylase and lipase) were diminished, and kidney dysfunction was evident, marked by elevated urea, creatinine, uric acid, and potassium levels, and decreased sodium concentrations. Histological analysis revealed significant collagen deposition in pancreatic tissue, indicative of fibrosis.
Ser treatment demonstrated protective effects by lowering serum glucose and HbA1c levels, restoring insulin and C-peptide concentrations, and enhancing antioxidant defenses. It reduced oxidative stress markers, pro-inflammatory mediators, and fibrosis in serum and pancreatic tissues. Additionally, digestive enzyme activities were restored, and kidney function improved, with normalization of urea, creatinine, uric acid, potassium, and sodium levels. Histological analysis confirmed reduced fibrosis and collagen deposition in the pancreatic tissue of Ser-treated rats.
These findings highlight sericin's potential to mitigate fibrosis and its associated complications in STZ-induced diabetic rats, offering promising therapeutic insights for managing diabetes-related organ damage.