Benefits of rutin on mitochondrial function and inflammation in an aluminum-induced neurotoxicity rat model: Potential interest for the prevention of neurodegeneration

• Published in: Biochimie 2024-07, Vol.222, p.1-8
• Main Authors: Kessas, Khadidja, Lounis, Wafaa, Chouari, Zehor, Vejux, Anne, Lizard, Gérard, Kharoubi, Omar
• Format: Article
• Language: English
• Subjects: Aluminum; Aluminum - toxicity; Aluminum Chloride - toxicity; Animals; Antioxidants - metabolism; Antioxidants - pharmacology; Brain - drug effects; Brain - metabolism; Brain - pathology; Disease Models, Animal; Inflammation - chemically induced; Inflammation - drug therapy; Inflammation - metabolism; Lipid Peroxidation - drug effects; Male; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Neuro-inflammation; Neurodegenerative Diseases - chemically induced; Neurodegenerative Diseases - drug therapy; Neurodegenerative Diseases - metabolism; Neurodegenerative Diseases - prevention & control; Neurotoxicity Syndromes - drug therapy; Neurotoxicity Syndromes - metabolism; Neurotoxicity Syndromes - prevention & control; Oxidative stress; Oxidative Stress - drug effects; Rat; Rats; Rats, Wistar; Rutin; Rutin - pharmacology; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 0300-9084; 1638-6183
• DOI: 10.1016/j.biochi.2024.02.010

Rutin, a phenolic compound, exhibits a diverse range of biological properties, including antioxidant, anti-inflammatory, and antimicrobial effects. In this study, we aimed to investigate the potential of rutin, a naturally occurring plant bioactive molecule, to mitigate the neurotoxic effects induced by aluminum chloride (AlCl3). Over a period of 6 weeks, rats were intraperitoneally injected with AlCl3 at a weekly dose of 60 mg/kg, while rutin treatment was administered orally via gavage at a daily dose of 30 mg/kg. AlCl3 exposure resulted in a significant increase lipid peroxidation (LPO) by 316.24%, nitrate levels by 504.14%, and tumor necrosis factor-alpha (TNF-α) levels by 93.82% in brain mitochondria. Additionally, AlCl3 exposure led to a reduction in glutathione levels and the activity of antioxidant enzymes, including superoxide dismutase (SOD) by 19.74%, glutathione peroxidase (GPx) by 44.76%, and catalase by 50.50%. There was also a significant decline in the activity of mitochondrial complex enzymes. In contrast, rutin treatment significantly enhanced the activity of antioxidant enzymes while concurrently reducing lipid peroxidation levels in rats. Specifically, rutin administration exerted a modulatory effect on the inflammatory response triggered by aluminum exposure, effectively suppressing the excessive production of nitrate and TNF-α. These findings highlight the potential of rutin as an effective therapeutic strategy in mitigating and combating neuro-inflammation and oxidative stress associated with aluminum-induced toxicity, thereby effectively restoring mitochondrial function. •Ivestigating dietary polyphenols' impact on brain functions, combating oxidative stress and inflammation in neurodegenerative rodent models.•Exploring the influence of dietary polyphenols on neuronal processes, promoting cerebral health by regulating mitochondrial function and inflammation.•Highliting rutin's therapeutic potential in relieving neuro-inflammation and oxidative stress caused by aluminum toxicity, restoring mitochondrial function effectively.