Ferulic acid mitigated rotenone toxicity -Evoked Parkinson in rat model by featuring apoptosis, oxidative stress, and neuroinflammation signaling

• Published in: Tissue & cell 2024-12, Vol.91, p.102614, Article 102614
• Main Authors: Youssef, Ola Mohammed, Lashine, Nermeen Hosney, El-Nablaway, Mohammad, El-yamany, Mona Ibrahim, Youssef, Manar Monir, Arida, Dina Abdalla
• Format: Article
• Language: English
• Subjects: alpha-Synuclein - metabolism; Animals; Apoptosis; Apoptosis - drug effects; Cerebellum - drug effects; Cerebellum - metabolism; Cerebellum - pathology; Coumaric Acids - pharmacology; Disease Models, Animal; Ferulic acid; Male; Neuroinflammatory Diseases - drug therapy; Neuroinflammatory Diseases - metabolism; Neuroprotective Agents - pharmacology; NF-kappa B - metabolism; Oxidative stress; Oxidative Stress - drug effects; Parkinson; Parkinson Disease - drug therapy; Parkinson Disease - etiology; Parkinson Disease - metabolism; Parkinson Disease - pathology; Rats; Rotenone; Rotenone - toxicity; Signal Transduction - drug effects
• ISSN: 0040-8166; 1532-3072; 1532-3072
• DOI: 10.1016/j.tice.2024.102614

Over time, Parkinson disease (PD) develops as a neurological illness. The goal of this study was to see whether ferulic acid has any neuroprotective benefits on the cerebellum of rats that have Parkinson's disease brought on by rotenone poisoning. A total of twenty-four male albino rats, in good condition, weighed between 200 and 250 g and nine to ten weeks old, were employed in the investigation. The control group received 1 ml of sunflower oil intraperitoneally (i.p.) each day. Rats' motor performance was considerably worse when given rotenone than it was in the control group. Rats given Ferulic Acid (FA) showed a substantial drop in the amount of glutathione (GSH) in the cerebellum. Moreover, the injection of FA resulted in a significant reduction in the optical density (OD) of the immune-positive reaction for α-synuclein, and the area percentage of BCL-2 and NF-kB immunological positive response. FA therapy, surprisingly, enhanced the OD of TH immunopositive response and apoptotic regulators (BCL2) in the cerebellum. Furthermore, FA boosted BCL2 expression, confirming the antiapoptotic effects of FA. Based on these results, FA is probably a good candidate to treat neurodegenerative diseases brought on by long-term exposure to rotenone. •Parkinson disease is a complex disease that involves multiple pathways.•The role of apoptosis, oxidative stress and neuroinflammation in the development of Parkinson disease.•Histological and biomolecular changes related to ferulic acid neuroprotective effect.•How Ferulic acid inhibits apoptosis, oxidative stress and neuroinflammation signaling which may contribute to its neuroprotective effect.