Ginkgo biloba extract mitigates the neurotoxicity of AlCl 3 in alzheimer rat's model: role of apolipoprotein E4 and clusterin genes in stimulating ROS generation and apoptosis.

Autor: Batawi AH; Department of Biological Science, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia.
Jazyk: angličtina
Zdroj: The International journal of neuroscience [Int J Neurosci] 2024 Jun; Vol. 134 (1), pp. 34-44. Date of Electronic Publication: 2022 Jun 09.
DOI: 10.1080/00207454.2022.2082968
Abstrakt: Purpose: Alzheimer's disease (AD) appears as a result of an increase in the accumulation of amyloid beta peptide (Aβ) and a decrease in neurotransmitters (acetylcholine) within the brain cells which may be due to increase in acetylcholinesterase (AchE) activity and change in expression of Apolipoprotein E4 (ApoE4) and Clusterin (Clu) genes. The aim of the present study was using natural products such as Ginkgo biloba ( G. biloba ) extract that has the potential to reduce Aβ formation and increase AchE inhibition with its ability to save neuronal DNA from damage.
Methods: Sixty male aged rats were divided into six experimental groups exposed to AlCl 3 to induce AD model and were treated with G. biloba extract. Collected brain tissues were used to assess the apoptosis rate, reactive oxygen species (ROS) generation, AchE inhibitory activity, expression alteration in ApoE4 and Clu genes, DNA fragmentations and gutathione peroxidase (GPx) activity. Results: The results exhibited that rats exposed to AlCl 3 increased significantly rate of apoptosis, ROS formation, DNA fragmentation, up-regulation of ApoE4 and Clu genes as well as decrease of AchE inhibitory activity and GPx activity compared with those in control rats. However, treatment of AlCl 3 -rats with G. biloba extract improved the above neurotoxicity results induced by AlCl 3 exposure.
Conclusions: It is therefore likely that G. biloba extract's protective properties against AD are due to its ability to activate the response against oxidative stress.
Databáze: MEDLINE
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