Prohibitive Effects of ω‐3 on Pancreatic Damage in an Experimental Diabetes Model: Blood Glucose, Insulin, Lipid Profiles, Oxidative Stress, Inflammation, Pancreatic Tissue Morphology, and Apoptotic Pathways

This study aimed to investigate the potential protective effects of Omega‐3 (ω−3) against damage to pancreatic tissue in rats with experimentally induced diabetes using streptozotocin. Twenty‐eight male Wistar Albino rats were divided into four groups: Control, Diabetes Mellitus (DM), ω−3, and DM + ω−3, with seven rats in each group. STZ was injected intraperitoneally (i.p.) into the DM group, and blood glucose levels were measured on the fourth day after injection. Rats with blood glucose levels of ≥ 200 mg/dL were diagnosed with DM. The ω−3 group received 500 mg/kg of ω−3. After the 42‐day experiment, pancreatic tissue and blood samples were collected from the rats. The DM group showed increased levels of malondialdehyde (MDA), total oxidant status (TOS), oxidative stress index (OSI), tumor necrosis factor α (TNF‐α), interleukin‐6 (IL‐6), glucose, LDL, triglycerides, caspase‐3 immunoreactivity, and histopathological abnormalities in pancreatic tissue. At the same time, there were decreases in superoxide dismutase (SOD), catalase (CAT), total antioxidant status (TAS), HDL, and insulin levels. Blood, biochemical, histopathological, and immunohistochemical parameters negatively impacted by ω−3 administration have improved. This study demonstrated that in STZ‐induced DM rats, DM increased oxidative capacity and led to oxidative stress, inflammation, apoptosis, and tissue damage. It was found that ω−3 has strong antioxidant, pro‐apoptotic, anti‐inflammatory, and protective effects.