Hesperidin attenuates altered redox homeostasis in an experimental hyperlipidemic model of rat.
Clin Exp Pharmacol Physiol. 2019 Dec 2. Epub 2019 Dec 2. PMID: 31793010
Diets rich in saturated fats, and cholesterol contribute to the incidence of hyperlipidemia. 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 thirty days) to induce an experimental hyperlipidemic model. HFD fed rats were also supplemented with hesperidin (100mg/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 defense parameters: ferric reducing ability of plasma (FRAP), reduced glutathione (GSH), Paraoxonase-1(PON-1 ), plasma membrane redox system (PMRS); general biochemical parameters: triglyceride, cholesterol , SGOT (serum glutamic oxaloacetic transaminase), and SGPT (serum glutamic pyruvic transaminase), fasting insulin, fasting glucose, Homa-IR index (Homeostatic model assessment -Insulin resistance), and inflammatory biomarkers: IL-6 and TNF-α. Experimental hyperlipidemia was found to be associated with significantly higher body weight (27.58 %), cholesterol (140 %), triglyceride (190 %), and fasting glucose level (37 %). ROS 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<0.05) 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 hyperlipidemia in rats.