Hyperlipidemia Downregulate Brain Antioxidant Defense Enzymes and Neurotrophins in Rats: Assessment of the Modulatory Potential of EPA+DHA and Zerumbone. Issue 20 (29th September 2020)

• Record Type: Journal Article
• Authors: Uppin, Vinayak; Acharya, Pooja; Bettadaiah Bheemanakere, Kempaiah; Talahalli, Ramaprasad Ravichandra
• Is Part Of: Molecular nutrition & food research. Volume 64:Issue 20(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-09-29
• Subjects: brain -- docosahexaenoic acid -- eicosapentaenoic acid -- hyperlipidemia -- oxidative stress -- zerumbone; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.202000381
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : Background: Oxidative stress (OS) plays a vital role in the pathogenesis of cognitive disorders. In this study, brain antioxidant defense dysregulation as a consequence of hyperlipidemia, and the efficacy of eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA), and zerumbone (Z) in their modulation are assessed. Methods and results: Male Wistar rats are fed control, high‐fat (HF), HF + fish oil (HF+F), HF + zerumbone (HF+Z), and HF + fish oil + zerumbone (HF+F+Z) diet for 60 days. Markers of OS, antioxidant enzymes, monoamine oxidase, nuclear factor (erythroid‐derived 2)‐like 2 (NRF‐2), nitric oxide‐2 (NOS‐2), inter cellular adhesion molecule‐1 (ICAM‐1), and neurotrophins are measured. Hyperlipidemia increases OS, decreases antioxidant enzyme activity, increases monoamine oxidase activity, increases NOS‐2 and ICAM‐1 expression, decreases NRF‐2 activation, decreases nerve growth factor (NGF), and brain‐derived neurotrophic factor (BDNF) levels in the brain compared to control. While EPA+DHA and zerumbone significantly ( p < 0.05) restores the perturbations induced by hyperlipidemia. Conclusion: It is concluded that hyperlipidemia cause OS by decreasing the activity of brain antioxidant enzymes via the downregulation of NRF‐2. The reduced brain neurotrophins in hyperlipidemia indicate its potential risk on cognitive attributes. EPA+DHA, together with zerumbone, positively modulates hyperlipidemia induced brain dysfunction thereby offering promising therapeutic strategy. Abstract : A) Hyperlipidemia mediated oxidative stress and its implication on brain function. B) Intervention of hyperlipidemia mediated oxidative stress and brain function by eicosapentaenoic acid + docosahexaenoic acid (EPA+DHA) and zerumbone.