article · Toxicology Reports
This research investigates the protective effects of fisetin, a natural flavonoid with antioxidant and anti-inflammatory properties, against neurodegeneration caused by aluminium chloride in adult male rats. Aluminium exposure is linked to neurological conditions such as Parkinson's disease, autism, and Alzheimer's disease. Rats were orally administered varying doses of fisetin either alone or as a pretreatment prior to aluminium chloride exposure. The exposure to aluminium chloride caused increased lipid peroxidation, reduced antioxidant activity, altered thalamic tissue structure, and raised markers of astrocyte and microglial activation. Pretreatment with fisetin mitigated these damaging effects, restoring antioxidant activity, reducing neuroinflammation markers, and preserving thalamic morphology. Overall, the findings demonstrate that fisetin counteracts aluminium chloride-induced neurodegeneration by regulating oxidative stress and inflammatory pathways in animal models.
Aluminium exposure is associated with debilitating neurological conditions such as Alzheimer's and Parkinson's diseases. Identifying natural compounds like fisetin that counteract cellular damage and inflammation provides crucial insights into how dietary flavonoids can protect brain cells, potentially informing future strategies for managing or preventing toxin-induced neurodegenerative disorders.
This work points toward the potential development of fisetin as a neuroprotective nutraceutical or therapeutic agent for individuals exposed to neurotoxic metals or facing neurodegenerative risks. The research remains at an early, preclinical stage, having only been demonstrated in laboratory rat models. Substantial further investigation, including toxicity testing, clinical trials, and formulation development, would be required before any commercial application or clinical use can be realised.
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Aim: Natural flavonoids have powerful antioxidant and anti-inflammatory activities against neurodegenerative diseases. Fisetin is a powerful flavonoid that targets a variety of neurological disorders. Aluminum (Al) has been linked to several neurological conditions, such as Parkinsons disease, autism, and Alzheimer's disease (AD). This study was designed to assess the modulatory role of fisetin in reversing oxidative stress and neuroinflammation caused by Aluminum chloride (AlCl3) induced neurological conditions in rats. Methods: Adult male Wistar were randomly divided into eight groups of four animals per group. Group 1; the control group received phosphate-buffered saline, group 2 received 100 mg/kg/bodyweight of aluminum chloride, and group 3,4, and 5 received 25, 50, and 75 mg/kg/bodyweight of fisetin respectively for 21 days. Groups 6, 7, and 8 received 25, 50, and 75 mg/kg/bodyweight of fisetin for 14 days followed by 100 mg/kg/bodyweight of aluminum chloride for 7 days respectively. The administration was via the oral route. Following treatment, the rats were euthanized, and biochemical alterations were observed by measuring the serum levels of Glutathione S-Transferase (GST) and Malondialdehyde (MDA) for oxidative stress and Interleukin-6 (IL-6) for neuroinflammation. Furthermore, histopathological evaluations of the thalamus were carried out using routine Hematoxylin and Eosin (H&E) and Cresyl Fast Violet (CFV) techniques while expressions of Glial Fibrillary Acidic Protein (GFAP) for astrocytes, and Ionized Calcium Binding Adapter Molecule 1 (IBA1) for microglia, were examined by immunohistochemical methods. Results: group indicated a rise in lipid peroxidation, decreased antioxidant activity, altered thalamic histomorphology, and increased expression of GFAP and IBA1 markers for astrocytes and microglia, respectively. These effects were mitigated in the Fisetin pretreated groups. Conclusion: -induced neurodegeneration possibly by mitigating oxidative stress and neuroinflammation.
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DOI: 10.1016/j.toxrep.2024.101812
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