Jana Kamel Bashraheel, Zienab A Alrefaie, Hossam Eldin Ahmed Awad Hammad, Soad Shaker Ali
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It also aimed to compare the protective effects of protective versus therapeutic effects of Vitamin D3 regiments on the number of degenerated neurons and the neuronal layer thickness.</p><p><strong>Materials and methods: </strong>Twenty-four adult male Albino Wister rats were sorted into GI: control; GII: AlCl<sub>3</sub>-AD model (100 mg/kg) orally for 42 days; GIII: Rats were co-treated with AlCl<sub>3</sub> (as GII) and Vitamin D<sub>3</sub> (400 IU/kg/day) orally for 42 days; GIV: Rats were treated with AlCl<sub>3</sub> for 42 days then with Vitamin D<sub>3</sub> for further 2 weeks. Sagittal sections (5 μ) from paraffin-processed brains previously fixed in 10% neutral-buffered formalin were stained with hematoxylin and eosin to evaluate the thickness and number of degenerated neurons in the hippocampal CA1, CA2, and CA3 subregions.</p><p><strong>Statistical analysis: </strong>The results of this study were expressed as mean ± standard deviation and analyzed by using IBM SPSS Statistics for Windows, version 23 (IBM SPSS, IBM Corp., Armonk, N.Y., USA). <i>P</i> < 0.05 was considered statistically significant.</p><p><strong>Results: </strong>Vitamin D<sub>3</sub> supplementations modulated the degenerative changes observed in the hippocampus of AD rat model. In all hippocampal subregions, the thickness was higher in rats treated with Vitamin D<sub>3</sub> after the AD induction than rats treated with Vitamin D<sub>3</sub> during AD induction. However, this increase was only significant in CA2. Comparison of the number of degenerated neurons between both groups treated with Vitamin D<sub>3</sub> revealed that in CA1, the number of degenerated neurons did not statistically differ between the two groups. However, it was insignificantly lower in CA2 in rats treated with Vitamin D<sub>3</sub> after the AD induction, and in CA3, it was insignificantly lower in rats treated with Vitamin D<sub>3</sub> during the AD induction.</p><p><strong>Conclusions: </strong>Vitamin D<sub>3</sub> was found to be effective in ameliorating histological and morphometric alterations in AlCl<sub>3</sub>-induced AD in rat model and could be proposed as both preventive and therapeutic supplements in high-risk AD patients.</p>","PeriodicalId":16340,"journal":{"name":"Journal of Microscopy and Ultrastructure","volume":"11 1","pages":"52-59"},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2a/04/JMAU-11-52.PMC10153740.pdf","citationCount":"1","resultStr":"{\"title\":\"The Possible Effects of Vitamin D3 on AlCl<sub>3</sub>-Induced Histological and Morphometric Alterations of Adult Male Albino Rat Hippocampus.\",\"authors\":\"Jana Kamel Bashraheel, Zienab A Alrefaie, Hossam Eldin Ahmed Awad Hammad, Soad Shaker Ali\",\"doi\":\"10.4103/jmau.jmau_42_21\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Context: </strong>Alzheimer's disease (AD) is a challenging neurodegenerative disease, and Vitamin D was proved to have neuroprotective effects.</p><p><strong>Aim: </strong>This study was conducted to evaluate the potential neuroprotective effects of Vitamin D3 supplementation on AlCl<sub>3</sub>-induced AD rat model in different hippocampal subregions (CA1, CA2, and CA3). 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引用次数: 1
摘要
背景:阿尔茨海默病(AD)是一种具有挑战性的神经退行性疾病，维生素D被证明具有神经保护作用。目的:本研究旨在评估补充维生素D3对alcl3诱导的AD大鼠模型不同海马亚区(CA1、CA2和CA3)的潜在神经保护作用。它还旨在比较维生素D3对退行性神经元数量和神经元层厚度的保护作用和治疗作用。材料与方法:将24只成年雄性白化Wister大鼠分为GI组，对照组;GII: AlCl3-AD模型(100 mg/kg)，口服42 d;GIII:大鼠口服AlCl3(作为GII)和维生素D3 (400 IU/kg/天)共治疗42天;GIV:大鼠用AlCl3治疗42天，再用维生素D3治疗2周。用苏木精和伊红对石蜡处理的大脑矢状面切片(5 μ)进行染色，以评估海马CA1、CA2和CA3亚区退化神经元的厚度和数量。统计分析:本研究结果以均数±标准差表示，采用IBM SPSS Statistics for Windows, version 23 (IBM SPSS, IBM Corp.， Armonk, n.y.， USA)进行分析。P < 0.05为差异有统计学意义。结果:维生素D3对AD大鼠海马退行性改变有调节作用。在所有海马亚区，AD诱导后维生素D3处理的大鼠的厚度都高于AD诱导期间维生素D3处理的大鼠。然而，这种增加仅在CA2中显着。比较维生素D3处理组与对照组在CA1中退行性神经元的数量，两组间的差异无统计学意义。然而，在AD诱导后，维生素D3处理的大鼠CA2水平不显著降低，在AD诱导过程中，维生素D3处理的大鼠CA3水平不显著降低。结论:维生素D3可有效改善alcl3诱导AD大鼠模型的组织学和形态学改变，可作为高风险AD患者的预防和治疗补充剂。
The Possible Effects of Vitamin D3 on AlCl3-Induced Histological and Morphometric Alterations of Adult Male Albino Rat Hippocampus.
Context: Alzheimer's disease (AD) is a challenging neurodegenerative disease, and Vitamin D was proved to have neuroprotective effects.
Aim: This study was conducted to evaluate the potential neuroprotective effects of Vitamin D3 supplementation on AlCl3-induced AD rat model in different hippocampal subregions (CA1, CA2, and CA3). It also aimed to compare the protective effects of protective versus therapeutic effects of Vitamin D3 regiments on the number of degenerated neurons and the neuronal layer thickness.
Materials and methods: Twenty-four adult male Albino Wister rats were sorted into GI: control; GII: AlCl3-AD model (100 mg/kg) orally for 42 days; GIII: Rats were co-treated with AlCl3 (as GII) and Vitamin D3 (400 IU/kg/day) orally for 42 days; GIV: Rats were treated with AlCl3 for 42 days then with Vitamin D3 for further 2 weeks. Sagittal sections (5 μ) from paraffin-processed brains previously fixed in 10% neutral-buffered formalin were stained with hematoxylin and eosin to evaluate the thickness and number of degenerated neurons in the hippocampal CA1, CA2, and CA3 subregions.
Statistical analysis: The results of this study were expressed as mean ± standard deviation and analyzed by using IBM SPSS Statistics for Windows, version 23 (IBM SPSS, IBM Corp., Armonk, N.Y., USA). P < 0.05 was considered statistically significant.
Results: Vitamin D3 supplementations modulated the degenerative changes observed in the hippocampus of AD rat model. In all hippocampal subregions, the thickness was higher in rats treated with Vitamin D3 after the AD induction than rats treated with Vitamin D3 during AD induction. However, this increase was only significant in CA2. Comparison of the number of degenerated neurons between both groups treated with Vitamin D3 revealed that in CA1, the number of degenerated neurons did not statistically differ between the two groups. However, it was insignificantly lower in CA2 in rats treated with Vitamin D3 after the AD induction, and in CA3, it was insignificantly lower in rats treated with Vitamin D3 during the AD induction.
Conclusions: Vitamin D3 was found to be effective in ameliorating histological and morphometric alterations in AlCl3-induced AD in rat model and could be proposed as both preventive and therapeutic supplements in high-risk AD patients.
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