ArticleFrontiers in pharmacology2025
Ferulic acid mitigates 3-Nitropropionic acid-induced Huntington's disease via modulation of Nrf2/HO-1, TLR4/NF-κB, and SIRT1/p53 signaling pathways.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Elucidating the Protective Potential of Ferulic Acid Against Sodium Arsenite- Induced Thyroid and Adrenal Toxicity: An Integrated In-Silico Molecular Docking and In-Vivo Experimental Approach.Biological trace element research · 2026Article
- Dietary Whole Wheat Flour Intake in Pakistan: A Cross-Sectional Insight into Long-Term Dementia Prevention.Nutrients · 2026Article
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10 authors.
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Abstract
Background: Ferulic acid (FA) is a natural phenolic compound that has demonstrated effectiveness against Huntington's disease (HD). However, its exact mechanism remains unclear. Therefore, the current study aims to investigate FA's potential mechanism of action against 3-nitropropionic acid (3NP)-induced HD. Methods: Adult male Wistar albino rats were administered FA orally (100 mg/kg) for 3 weeks, and 3NP (10 mg/kg) was intraperitoneally administered during the last 2 weeks to induce HD. Behavioral performance was assessed using the open field and hanging wire tests. Striatal tissue was analyzed using ELISA, qRT-PCR, Western blotting, histopathology, and immunohistochemistry. Results: Administration of 3NP led to weight loss, neurobehavioral deficits, oxidative damage, apoptotic cell death, and neuroinflammation. FA treatment mitigated these pathological changes by activating Nrf2/HO-1 signaling, a critical player in cellular redox balance. This beneficial effect was mirrored in restoring TAC levels and suppressing MDA. Moreover, FA suppressed TLR4/NF-κB inflammatory signaling, thereby reducing TNF-α and IL-1β levels. In addition, the anti-apoptotic properties of FA were confirmed by modulating SIRT1/p53 signaling, leading to Bcl-2 enhancement and caspase-3 downsizing. Furthermore, FA enhanced neuronal survival and plasticity confirmed by neurotrophic BDNF elevation. Histopathological and immunohistochemical analyses confirmed improved neuronal survival and reduced gliosis following FA treatment. Conclusion: The current research demonstrates that FA exhibits potent neuroprotective effects in experimental HD by modifying Nrf2/HO-1, TLR4/NF-κB, and SIRT1/p53 signaling pathways. These findings provide new mechanistic insights into FA's potential role in managing HD.
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