Comparative Study on the Influence of Epigallocatechin-3-gallat e and/ or Coenzyme Q10 against Alzheimer's disease Induced by Aluminium in Normally-Fed and Protein Malnourished Rats
- *Corresponding Author:
- Azza A Ali
Prof and Head of Pharmacology and Toxicology Department
Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt
Tel: +20 01061905439
E-mail: [email protected]
Received date: May 19, 2016; Accepted date: June 08, 2016; Published date: June 15, 2016
Citation: Ali AA, Ahmed HI, Khalil MG, Alwakeel AI, Elfotuh KA (2016) Comparative Study on the Influence of Epigallocatechin-3-gallate and/or Coenzyme Q10 against Alzheimer’s disease Induced by Aluminium in Normally-Fed and Protein Malnourished Rats. J Alzheimers Dis Parkinsonism 6:240. doi:10.4172/2161-0460.1000240
Copyright: © 2016 Ali AA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Alzheimer’s disease (AD) is a neurodegenerative disorder greatly influenced by oxidative stress and mitochondrial dysfunction which may lead to deposition of β-amyloid (Aβ) peptides. Protein malnutrition increases oxidative damage in cortex, hippocampus and cerebellum. Epigallocatechin-3-gallate (EGCG) has health-promoting effects in CNS, while Coenzyme Q10 (CoQ10) is intracellular antioxidant and mitochondrial membrane stabilizer.
Objective: To investigate the possible protective effect of EGCG and/or CoQ10 against aluminium-induced neurotoxicity presenting symptoms that mimic AD in both normally-fed (NF) and protein malnourished (PM) rats.
Methods: Ten groups of rats were used; five for NF (20% casein) and the same for PM (10% casein). Both NF and PM groups received daily for four weeks; either saline for control or AlCl3 (70 mg/kg, I.P) for AD induction groups, treated groups received together with AlCl3 either EGCG (10 mg/kg, I.P), CoQ10 (200 mg/kg, P.O) or combination of both. Histopathological changes in the brain and biochemical changes in Aβ, Acetyl cholinesterase (ACHE) as well as oxidative parameters (MDA, SOD, TAC) were evaluated for all groups.
Results: The study revealed that, brain neurological damage characterizing induction of AD as indicated by histopathological changes in the brain and the increase in Aβ, ACHE and MDA as well as the decrease in SOD and TAC was more pronounced in PM rats. Administration of EGCG and/or CoQ10 during induction of AD showed protective effect in both NF and PM rats as indicated by the decreased Aβ, ACHE, MDA together with the increased SOD, TAC and confirmed by histo pathological examinations in different brain regions. However, the effect of combined treatment was more pronounced in both NF and PM rats.
Conclusion: PM is a risk factor in induction of AD, EGCG and CoQ10 combined therapy has marked protective effects during induction of AD in both NF and PM rats rather than each individual treatment.