Emodin attenuates insulin resistance in the gastrocnemius muscle by modulating the expression of IL-1βTNF-α/NF-kB-mediated signalling in streptozotocin-induced diabetic Rats

Diabetes mellitus, particularly type 2 diabetes (T2DM), is characterized by insulin resistance, oxidative stress, and inflammation, which contribute to metabolic dysfunction. This study aimed to evaluate the effects of emodin on oxidative stress, inflammatory cytokines, and insulin signaling in a Streptozotocin (STZ)-induced diabetic rat model. Type 2 diabetes was induced by an intraperitoneal injection of streptozotocin (35 mg/kg body weight in 0.1 M citrate buffer, pH 4.5). The rats were divided into five groups, each consisting of six animals: Group I (normal rats, vehicle control), Group II (Type 2 diabetic rats), Group III (Type 2 diabetic rats treated with Emodin at 40 mg/kg b.wt/day orally for 45 days), Group IV (Type 2 diabetic rats treated with metformin), and Group V (control with Emodin). Emodin treatment significantly reduced oxidative stress markers (H₂O₂: 32±2.45 μm, OH: 40±2.9 μm), restored antioxidant enzyme activities (CAT: 15±0.84 ng/L, GPX: 27±1.8 pmol/ml), and reduced inflammatory cytokines (TNF-α: 180±11.64 pg/ml, IL-1β: 360±28.63 pg/ml, NF-kB: 140±8.9 ng/L). Additionally, emodin treatment enhanced the expression of insulin signaling molecules, including IR, IRS-1, PI3K, AKT, GLUT4, and AS160, indicating improved insulin sensitivity. These findings suggest that emodin can modulate oxidative stress, inflammation, and insulin resistance, providing a promising therapeutic approach for type 2 diabetes. Further studies are necessary to explore its clinical relevance and underlying molecular mechanisms.