Protective Role of Fargesin in Streptozotocin-induced Diabetic Mice for Wound Healing via Alteration of NF-κB/VEGF and HO-1/Nrf2 Signaling Pathway

Background Diabetes mellitus (DM) is a metabolic disorder that has exhibited a significant rise in global incidence in recent years. Purpose Our study aims to investigate the wound-protective effect of fargesin against streptozotocin (STZ)-induced wounds in rats and to explore the underlying mechanism. Materials and Methods Intraperitoneal administration of STZ was used for the induction of DM in rats, and rats were randomized into five groups as follows: Gp I: normal control, Gp II: diabetic control group untreated wound, Gp III: diabetes and fargesin (5 mg/kg) treated wound, Gp IV: diabetes and fargesin (10 mg/kg) treated wound, and Gp V: diabetes and fargesin (20 mg/kg), respectively. Blood glucose level, insulin level, lipid parameters, collagen, hexosamine, macrophage migration inhibitory factor (MIF), nitric oxide (NO), epidermal growth factor (EGF), C-C motif chemokine ligand 2 (CCL-2), C-C motif chemokine ligand 3 (CCL-3), C-X-C motif chemokine ligand 2 (CXCL2), antioxidant parameters, inflammatory cytokines, inflammatory parameters, and mRNA expression were scrutinized. Results Fargesin treatment altered the levels of MIF, collagen, hexosamine, NO, EGF, C-C motif chemokine ligand (CCL2, CCL3), and CXCL2. Fargesin treatment decreased the glucose level and improved the insulin level. Fargesin treatment altered the level of lipid parameters, antioxidant, and inflammatory cytokines, namely, inflammatory parameters such as heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor 2 (Nrf 2 ). Fargesin treatment altered the mRNA expression of cytokines and inflammatory parameters. Conclusion In conclusion, oral administration of fargesin ameliorates wound healing via alteration of inflammation and oxidative stress through the regulation of nuclear factor kappa B (NF-κB)/vascular endothelial growth factor (VEGF) and HO-1/Nrf 2 signaling pathway.