Hesperidin attenuates altered redox homeostasis in an experimental hyperlipidaemic model of rat.

Diets rich in saturated fats and cholesterol contribute to the incidence of hyperlipidaemia. An altered lipid profile is a major factor responsible for the development of CVD. Male Wistar rats were fed with a high-fat diet (HFD) (suspension (w/v) of 0.5% cholesterol, 3% coconut oil and 0.25% cholic acid for 30 days) to induce an experimental hyperlipidaemic model. High-fat diet fed rats were also supplemented with hesperidin (100 mg/kg body weight). The present study reports reactive oxygen species (ROS) production, oxidative stress parameters: malondialdehyde (MDA), protein carbonyl (PCO), oxidation of plasma protein (AOPP), and advance glycation end products (AGEs); antioxidant defence parameters: ferric reducing ability of plasma (FRAP), reduced glutathione (GSH), Paraoxonase-1 (PON-1), plasma membrane redox system (PMRS); general biochemical parameters: triglyceride, cholesterol, serum glutamic oxaloacetic transaminase (SGOT), and serum glutamic pyruvic transaminase (SGPT), fasting insulin, fasting glucose, homeostatic model assessment-insulin resistance (Homa-IR) index, and inflammatory biomarkers: interleukin (IL)-6 and tumour necrosis factor (TNF)-α. Experimental hyperlipidaemia was found to be associated with significantly higher body weight (27.58%), cholesterol (140%), triglyceride (190%), and fasting glucose level (37%). Reactive oxygen species production (67%), MDA (28.9%), AOPP (31.42%), PCO (58.53%), and PMRS (156%), inflammatory markers, cytokines IL-6 and TNF-α, were elevated and GSH (50%), PON 1 (37.07%), and FRAP (26.58%) activity were significantly (P < .05) lower in the high-fat diet group. Hesperidin supplementation protected HFD-fed rats from oxidative damage. Our findings indicate that the supplementation of hesperidin provides protection against redox imbalance induced by hyperlipidaemia in rats.