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<p>Sodium butyrate is a histone deacetylase (HDAC) inhibitor, which regulates gene expression in the brain. We aimed to investigate the possible therapeutic effect of the HDAC inhibitor sodium butyrate alone or combined with vitamin E (Vit.E) in an experimental model of Alzheimer’s disease induced in the rat by aluminum chloride (AlCl<sub>3</sub>). Rats received subcutaneous injections of AlCl<sub>3</sub> (10&#xa0;mg/kg) daily for 8&#xa0;weeks. Starting from the 5th week of AlCl<sub>3</sub> administration, rats were also treated orally with sodium butyrate (50, 100, or 200&#xa0;mg/kg), Vit.E (25&#xa0;mg/kg), sodium butyrate (100&#xa0;mg/kg) + Vit.E (25&#xa0;mg/kg), or donepezil (10&#xa0;mg/kg). Malondialdehyde (MDA), paraoxonase-1 (PON-1) activity, nitric oxide (NO), reduced glutathione (GSH), acetylcholine esterase (AChE), nuclear factor kappa B (NFκB), interleukin-1 beta (IL-1β), and amyloid beta (Aβ<sub>1-42</sub>) were measured in brain tissue besides histopathology. Results indicated that compared with saline controls, AlCl<sub>3</sub>-injected rats exhibited significant increases in brain MDA, NO, AChE, IL-1β, NFκB, and Aβ<sub>1-42</sub> levels, along with significant decreases in PON-1 and GSH levels. Sodium butyrate administered to AlCl<sub>3</sub>-injected rats resulted in significant alleviation of oxidative stress and decreased Aβ-peptide, IL-1β, NFκB, and AChE. Vit.E or donepezil was also effective in lowering MDA and Aβ-peptide levels. Sodium butyrate alone or with Vit.E prevented neurodegeneration in the hippocampus and cerebral cortex of AlCl<sub>3</sub>-injected rats. Our results indicate that sodium butyrate exerts neuroprotective, anti-oxidative, anti-inflammatory, and Aβ-peptide lowering effects, suggesting a new treatment option for Alzheimer’s disease.</p>

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The ameliorative effect of sodium butyrate alone or combined with vitamin E on oxidative stress and neurodegeneration in an experimental model of Alzheimer’s disease

  • 期刊论文

  • 发表日期：

    2025年10月21日

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  • Soha Mohamed Hamdy,
  • Mai Bakkar Mekheimer,
  • Eman R. Youness,
  • Heba Mohamed Rabie Elesh,
  • Omar M. E. Abdel‑Salam

摘要

Sodium butyrate is a histone deacetylase (HDAC) inhibitor, which regulates gene expression in the brain. We aimed to investigate the possible therapeutic effect of the HDAC inhibitor sodium butyrate alone or combined with vitamin E (Vit.E) in an experimental model of Alzheimer’s disease induced in the rat by aluminum chloride (AlCl3). Rats received subcutaneous injections of AlCl3 (10 mg/kg) daily for 8 weeks. Starting from the 5th week of AlCl3 administration, rats were also treated orally with sodium butyrate (50, 100, or 200 mg/kg), Vit.E (25 mg/kg), sodium butyrate (100 mg/kg) + Vit.E (25 mg/kg), or donepezil (10 mg/kg). Malondialdehyde (MDA), paraoxonase-1 (PON-1) activity, nitric oxide (NO), reduced glutathione (GSH), acetylcholine esterase (AChE), nuclear factor kappa B (NFκB), interleukin-1 beta (IL-1β), and amyloid beta (Aβ1-42) were measured in brain tissue besides histopathology. Results indicated that compared with saline controls, AlCl3-injected rats exhibited significant increases in brain MDA, NO, AChE, IL-1β, NFκB, and Aβ1-42 levels, along with significant decreases in PON-1 and GSH levels. Sodium butyrate administered to AlCl3-injected rats resulted in significant alleviation of oxidative stress and decreased Aβ-peptide, IL-1β, NFκB, and AChE. Vit.E or donepezil was also effective in lowering MDA and Aβ-peptide levels. Sodium butyrate alone or with Vit.E prevented neurodegeneration in the hippocampus and cerebral cortex of AlCl3-injected rats. Our results indicate that sodium butyrate exerts neuroprotective, anti-oxidative, anti-inflammatory, and Aβ-peptide lowering effects, suggesting a new treatment option for Alzheimer’s disease.