Document Type : Original Article
Authors
1
Chemistry department , Faculty of Science, Fayoum University, Al Fayoum, Egypt
2
chemistrydepartment,faculty of science, fayoum university
3
Zoology Department, Faculty of Science, Fayoum University, Fayoum, Egypt
4
. National Research Center Department of Toxicology and Narcotics, National Research Centre, Tahrir St., Dokki, Cairo, Egypt
Abstract
Abstract
Aim: Alzheimer’s disease (AD), is linked to oxidative stress, which accelerates neuronal damage and cognitive decline. Sodium butyrate, has antioxidant properties and capacity to control gene expression, We aimed to study the potential therapeutic effect of the histone deacetylase (HDAC) inhibitor sodium butyrate alone or its combination with vitamin E (Vit.E) on oxidative stress biomarkers in an experimental model of (AD) induced by AlCl3 in the rat.
Methods: Rats injected with AlCl3 subcutaneously (10 mg/kg) daily for 8 weeks. From the 5th week of AlCl3injection afterwards, rats were administrated sodium butyrate (50,100 or 200 mg/kg), Vit.E (25 mg/kg), sodium butyrate (100 mg/kg) + Vit. E (25 mg/kg), and donepezil (10 mg/kg) orally along with AlCl3. Lipid peroxidation (malondialdehyde: MDA), reduced glutathione (GSH), and nitric oxide (NO) were measured in brain homoigenates.
Results: compared with the saline-treated control group, rats given AlCl3 showed significant and marked increases in brain NO and MDA levels, Meanwhile, GSH showed significant decrease when compared with the saline control group. The results of those parameters in AlCl3- injected rats treated with sodium butyrate showed significant improvement, also vit.E and donepezil were effective to reduce MDA and NO.
Conclusions: the results show that sodium butyrate has neuroprotective, and anti-oxidative roles which guide us to a new treatment for AD disease.
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