IGF 1, BDNF, and NGF mediate the neuro-modulatory role of stem cells in acrylamide-induced hippocampal toxic changes in rats.

IF 1.2 4区医学 Q3 ANATOMY & MORPHOLOGY

Folia morphologica Pub Date : 2024-09-18 DOI:10.5603/fm.101454

Nabila Youssef Abdel Halim, Gamal Hosny Mohamed, Ahmed Elhusseiny, Marwa Abdelgwad, Reda Abdelnasser Imam

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引用次数: 0

Abstract

Background: Acrylamide (ACR), a common industrial chemical, is a strong neurotoxic material. The hippocampus is a brain area of interest mostly affected by Alzheimer's disease. Mesenchymal stem cells (MSCs) usefulness in various neurological diseases including Alzheimer's is being debated. In this work, the authors aim to explore the role of MSCs in ACR-induced hippocampal neurodegeneration and elucidate the mediating mechanism.

Materials and methods: For this purpose, ten rats served as control, another ten were injected ACR (i.p. 50 mg/kg/day for 2 weeks), and the last ten rats were injected ACR in addition to MSCs (i.p. 1 × 10⁷ MSCs single injection).

Results: ACR induced neurodegenerative histopathological hippocampal changes and adversely altered hippocampal oxidative stress markers SOD, MDA, and GSH. ACR had induced hippocampal demyelination as detected by silver staining. ACR significantly (P < 0.05) up-regulated the ELISA hippocampal TNF-alpha and IL-6 and produced microglial & astrocyte activation (as tracked by Iba1 & GFAP immunohistochemistry respectively). ACR significantly reduced hippocampal PCR gene expression of IGF 1 (insulin growth factor-1), BDNF (brain-derived neurotrophic factor), and NGF (nerve growth factor). MSCs administration had mitigated all the previous deleterious changes.

Conclusions: Acrylamide caused detrimental effects on the hippocampus and demonstrably altered the hippocampal architecture. Bone marrow mesenchymal stem cells offered a promising therapeutic role against these neurotoxic effects of acrylamide, presumably through modulation of IGF 1, BDNF, and NGF gene expressions.

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IGF 1、BDNF 和 NGF 在丙烯酰胺诱导的大鼠海马毒性变化中介导干细胞的神经调节作用。

背景：丙烯酰胺（ACR）是一种常见的工业化学品，具有很强的神经毒性。海马区是受阿尔茨海默病影响最严重的脑区。间充质干细胞（MSCs）在包括阿尔茨海默氏症在内的各种神经系统疾病中的作用一直备受争议。在这项工作中，作者旨在探索间充质干细胞在 ACR 诱导的海马神经退行性变中的作用，并阐明其介导机制：为此，10只大鼠作为对照组，另外10只大鼠注射ACR（静脉注射50毫克/千克/天，连续2周），最后10只大鼠在注射ACR的同时注射间充质干细胞（静脉注射1×10⁷间充质干细胞单次）：结果：ACR诱导神经退行性海马组织病理学改变，并对海马氧化应激标志物SOD、MDA和GSH产生不利影响。银染色法检测到 ACR 诱导了海马脱髓鞘。ACR 能明显（P < 0.05）上调 ELISA 海马 TNF-α 和 IL-6，并产生微胶质细胞和星形胶质细胞活化（分别通过 Iba1 和 GFAP 免疫组化追踪）。ACR 能明显降低海马 PCR 基因中 IGF 1（胰岛素生长因子-1）、BDNF（脑源性神经营养因子）和 NGF（神经生长因子）的表达。服用间充质干细胞可减轻之前的所有有害变化：结论：丙烯酰胺会对海马产生有害影响，并明显改变海马的结构。骨髓间充质干细胞可能通过调节 IGF 1、BDNF 和 NGF 基因的表达，对丙烯酰胺的这些神经毒性效应具有良好的治疗作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Folia morphologica ANATOMY & MORPHOLOGY-

CiteScore

2.40

自引率

0.00%

发文量

218

审稿时长

6-12 weeks

期刊介绍： "Folia Morphologica" is an official journal of the Polish Anatomical Society (a Constituent Member of European Federation for Experimental Morphology - EFEM). It contains original articles and reviews on morphology in the broadest sense (descriptive, experimental, and methodological). Papers dealing with practical application of morphological research to clinical problems may also be considered. Full-length papers as well as short research notes can be submitted. Descriptive papers dealing with non-mammals, cannot be accepted for publication with some exception.