The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats

Alzheimer’s disease (AD) is a worldwide rapidly growing neurodegenerative disease. Here, we elucidated the neuroprotective effects of silymarin (SM) on the hippocampal tissues of aluminum chloride (AlCl<sub>3</sub>)-induced Alzheimer-like disease in rats using biochemical, histological,...

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Main Authors: Hanaa R. Aboelwafa, Attalla F. El-kott, Eman M. Abd-Ella, Hany N. Yousef
Format: Article
Language:English
Published: MDPI AG 2020-09-01
Series:Brain Sciences
Subjects:
Online Access:https://www.mdpi.com/2076-3425/10/9/628
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author Hanaa R. Aboelwafa
Attalla F. El-kott
Eman M. Abd-Ella
Hany N. Yousef
author_facet Hanaa R. Aboelwafa
Attalla F. El-kott
Eman M. Abd-Ella
Hany N. Yousef
author_sort Hanaa R. Aboelwafa
collection DOAJ
description Alzheimer’s disease (AD) is a worldwide rapidly growing neurodegenerative disease. Here, we elucidated the neuroprotective effects of silymarin (SM) on the hippocampal tissues of aluminum chloride (AlCl<sub>3</sub>)-induced Alzheimer-like disease in rats using biochemical, histological, and ultrastructural approaches. Forty rats were divided into control, SM, AlCl<sub>3</sub>, and AlCl<sub>3</sub> + SM groups. Biochemically, AlCl<sub>3</sub> administration resulted in marked elevation in levels of lipid peroxidation (LPO) and nitric oxide (NO) and decrease in levels of reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Moreover, AlCl<sub>3</sub> significantly increased tumor necrosis factor-α (TNF-α), interleukin-1beta (IL-1β), and acetylcholinesterase (AChE) activities. Furthermore, myriad histological and ultrastructural alterations were recorded in the hippocampal tissues of AlCl<sub>3</sub>-treated rats represented as marked degenerative changes of pyramidal neurons, astrocytes, and oligodendrocytes. Additionally, some myelinated nerve fibers exhibited irregular arrangement of their myelin coats, while the others revealed focal degranulation of their myelin sheaths. Severe defects in the blood–brain barrier (BBB) were also recorded. However, co-administration of SM with AlCl<sub>3</sub> reversed most of the biochemical, histological, and ultrastructural changes triggered by AlCl<sub>3</sub> in rats. The results of the current study indicate that SM can potentially mend most of the previously evoked neuronal damage in the hippocampal tissues of AlCl<sub>3</sub>-kindled rats.
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spelling doaj.art-bd55e06672e146108958217ffac0c9d52023-11-20T13:20:03ZengMDPI AGBrain Sciences2076-34252020-09-0110962810.3390/brainsci10090628The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in RatsHanaa R. Aboelwafa0Attalla F. El-kott1Eman M. Abd-Ella2Hany N. Yousef3Department of Biological and Geological Sciences, Faculty of Education, Ain Shams University, Cairo 11566, EgyptBiology Department, Faculty of Science, King Khalid University, Abha 61421, Saudi ArabiaZoology Department, College of Science, Fayoum University, Fayoum 63514, EgyptDepartment of Biological and Geological Sciences, Faculty of Education, Ain Shams University, Cairo 11566, EgyptAlzheimer’s disease (AD) is a worldwide rapidly growing neurodegenerative disease. Here, we elucidated the neuroprotective effects of silymarin (SM) on the hippocampal tissues of aluminum chloride (AlCl<sub>3</sub>)-induced Alzheimer-like disease in rats using biochemical, histological, and ultrastructural approaches. Forty rats were divided into control, SM, AlCl<sub>3</sub>, and AlCl<sub>3</sub> + SM groups. Biochemically, AlCl<sub>3</sub> administration resulted in marked elevation in levels of lipid peroxidation (LPO) and nitric oxide (NO) and decrease in levels of reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Moreover, AlCl<sub>3</sub> significantly increased tumor necrosis factor-α (TNF-α), interleukin-1beta (IL-1β), and acetylcholinesterase (AChE) activities. Furthermore, myriad histological and ultrastructural alterations were recorded in the hippocampal tissues of AlCl<sub>3</sub>-treated rats represented as marked degenerative changes of pyramidal neurons, astrocytes, and oligodendrocytes. Additionally, some myelinated nerve fibers exhibited irregular arrangement of their myelin coats, while the others revealed focal degranulation of their myelin sheaths. Severe defects in the blood–brain barrier (BBB) were also recorded. However, co-administration of SM with AlCl<sub>3</sub> reversed most of the biochemical, histological, and ultrastructural changes triggered by AlCl<sub>3</sub> in rats. The results of the current study indicate that SM can potentially mend most of the previously evoked neuronal damage in the hippocampal tissues of AlCl<sub>3</sub>-kindled rats.https://www.mdpi.com/2076-3425/10/9/628Alzheimer’s diseasesilymarinhippocampusaluminum chlorideoxidative stresshistology
spellingShingle Hanaa R. Aboelwafa
Attalla F. El-kott
Eman M. Abd-Ella
Hany N. Yousef
The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats
Brain Sciences
Alzheimer’s disease
silymarin
hippocampus
aluminum chloride
oxidative stress
histology
title The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats
title_full The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats
title_fullStr The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats
title_full_unstemmed The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats
title_short The Possible Neuroprotective Effect of Silymarin against Aluminum Chloride-Prompted Alzheimer’s-Like Disease in Rats
title_sort possible neuroprotective effect of silymarin against aluminum chloride prompted alzheimer s like disease in rats
topic Alzheimer’s disease
silymarin
hippocampus
aluminum chloride
oxidative stress
histology
url https://www.mdpi.com/2076-3425/10/9/628
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