4.3 Article

Amelioration of Age-Related Multiple Neuronal Impairments and Inflammation in High-Fat Diet-Fed Rats: The Prospective Multitargets of Geraniol

Journal

OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2022, Issue -, Pages -

Publisher

HINDAWI LTD
DOI: 10.1155/2022/4812993

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Funding

  1. Deanship of Scientific Research at Jouf University
  2. [DSR2020-04-2561]

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The study investigates the effectiveness of geraniol in manipulating age- and diet-associated toxicity and neuroinflammation in rats fed with a high-fat diet. The results demonstrate that geraniol supplementation reduces inflammation, improves liver, kidney, and lipid profiles, decreases brain insulin resistance, suppresses acetylcholinesterase activity, alleviates oxidative stress, restores brain tissue damage, enhances learning and memory function, and lowers protein and gene expression levels associated with inflammation. Geraniol also reverses oxidative and inflammation changes associated with aging.
Neuroinflammation is documented to alter brain function as a consequence of metabolic changes linked with a high-fat diet (HFD). The primary target of this study is to see how geraniol is effective in manipulating age- and diet-associated multiple toxicity and neuroinflammation in HFD-fed rats. Sixty-four adult male Wistar rats were partitioned into two groups: Group 1 (untreated normal young and aged rats) and Group 2 (HFD-fed young and aged rats) that received HFD for 16 weeks before being orally treated with geraniol or chromax for eight weeks. The results revealed a dropping in proinflammatory cytokines (TNF-alpha and IL-6) and leptin while boosting adiponectin in geraniol-supplemented rats. The liver, kidney, and lipid profiles were improved in geraniol-HFD-treated groups. HFD-induced brain insulin resistance decreased insulin clearance and insulin-degrading enzyme (IDE) levels significantly after geraniol supplementation. Geraniol suppressed acetylcholinesterase (AChE) activity and alleviated oxidative stress by boosting neuronal reduced glutathione (GSH), catalase (CAT), glutathione-S-transferase (GST), and superoxide dismutase (SOD) activities. It lowered malondialdehyde concentration (TBARS), nitric oxide (NO), and xanthine oxidase (XO) and restored the structural damage to the brain tissue caused by HFD. Compared with model rats, geraniol boosted learning and memory function and ameliorated the inflammation status in the brain by lowering the protein levels of IL-1 beta, iNOS, NF-kappa Bp65, and COX-2. In addition, the expression levels of inflammation-related genes (MCP-1, TNF-alpha, IL-6, IL-1 beta, and IDO-1) were lessened significantly. Remarkably, the supplementation of geraniol reversed the oxidative and inflammation changes associated with aging. It affected the redox status of young rats. In conclusion, our results exhibit the effectiveness of dietary geraniol supplementation in modifying age-related neuroinflammation and oxidative stress in rats and triggering off the use of geraniol as a noninvasive natural compound for controlling age- and diet-associated neuronal impairments and toxicity.

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