Abstract Title:

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

Abstract Source:

Clin Exp Pharmacol Physiol. 2019 Dec 2. Epub 2019 Dec 2. PMID: 31793010

Abstract Author(s):

Raushan Kumar, Farhan Akhtar, Syed Ibrahim Rizvi

Article Affiliation:

Raushan Kumar


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.

Study Type : Animal Study

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