Regional Changes in Brain Biomolecular Markers in a Collagen-Induced Arthritis Rat Model

Biology Pub Date : 2024-07-10 DOI:10.3390/biology13070516

A. Millen, Tshiamo T. Maluleke, Leandrie Pienaar, Farhanah N. Sallie, Radhini Veerappan, P. Andren, S. Baijnath

{"title":"Regional Changes in Brain Biomolecular Markers in a Collagen-Induced Arthritis Rat Model","authors":"A. Millen, Tshiamo T. Maluleke, Leandrie Pienaar, Farhanah N. Sallie, Radhini Veerappan, P. Andren, S. Baijnath","doi":"10.3390/biology13070516","DOIUrl":null,"url":null,"abstract":"Background: The effects of collagen-induced arthritis (CIA), a model of systemic inflammation, on brain regional molecular markers associated with neurological disorders are uncertain. Objective: This study investigated the brain regional molecular changes in markers associated with inflammation and neuronal dysfunction in a CIA model. Methods: Fourteen male Sprague Dawley rats were divided into control (n = 5) or CIA (n = 9) groups. 10 weeks after CIA induction, brain tissue was collected. Brain regional mRNA expression of inflammatory markers (IL-1β and IL-6), apoptotic markers (BAX and Bcl2) and neurotrophic factors (BDNF, CREB and TrkB) was determined. Monoamine distribution and abundance in different brain regions were determine by mass spectrometry imaging (MSI). Results: Neuroinflammation was confirmed in the CIA group by increased IL-β mRNA expression, concurrent with an increased BAX/Bcl2 ratio. The mRNA expression of CREB was increased in the midbrain and hippocampus while BDNF was increased and TrkB was decreased across all brain regions in CIA compared to control animals. Serotonin was decreased in the midbrain and hippocampus while dopamine was decreased in the striatum of CIA rats, compared to controls. Conclusion: CIA resulted in neuroinflammation concurrent with an apoptotic state and aberrant expression of neurotrophic factors and monoamines in the brain, suggestive of neurodegeneration.","PeriodicalId":504576,"journal":{"name":"Biology","volume":"21 15","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/biology13070516","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 0

Abstract

Background: The effects of collagen-induced arthritis (CIA), a model of systemic inflammation, on brain regional molecular markers associated with neurological disorders are uncertain. Objective: This study investigated the brain regional molecular changes in markers associated with inflammation and neuronal dysfunction in a CIA model. Methods: Fourteen male Sprague Dawley rats were divided into control (n = 5) or CIA (n = 9) groups. 10 weeks after CIA induction, brain tissue was collected. Brain regional mRNA expression of inflammatory markers (IL-1β and IL-6), apoptotic markers (BAX and Bcl2) and neurotrophic factors (BDNF, CREB and TrkB) was determined. Monoamine distribution and abundance in different brain regions were determine by mass spectrometry imaging (MSI). Results: Neuroinflammation was confirmed in the CIA group by increased IL-β mRNA expression, concurrent with an increased BAX/Bcl2 ratio. The mRNA expression of CREB was increased in the midbrain and hippocampus while BDNF was increased and TrkB was decreased across all brain regions in CIA compared to control animals. Serotonin was decreased in the midbrain and hippocampus while dopamine was decreased in the striatum of CIA rats, compared to controls. Conclusion: CIA resulted in neuroinflammation concurrent with an apoptotic state and aberrant expression of neurotrophic factors and monoamines in the brain, suggestive of neurodegeneration.

查看原文本刊更多论文

胶原蛋白诱导的关节炎大鼠模型中脑生物分子标记物的区域变化

背景：胶原诱导的关节炎（CIA）是一种全身性炎症模型，它对与神经系统疾病相关的脑区域分子标记物的影响尚不确定。研究目的本研究调查了 CIA 模型中与炎症和神经元功能障碍相关的脑区分子标记物的变化。研究方法将 14 只雄性 Sprague Dawley 大鼠分为对照组（5 只）和 CIA 组（9 只）。诱导 CIA 10 周后收集脑组织。测定脑区炎症标志物（IL-1β和IL-6）、凋亡标志物（BAX和Bcl2）和神经营养因子（BDNF、CREB和TrkB）的mRNA表达。通过质谱成像（MSI）测定了单胺在不同脑区的分布和丰度。结果显示CIA组的IL-β mRNA表达增加，同时BAX/Bcl2比率增加，证实了神经炎症。与对照组相比，CIA 组动物中脑和海马的 CREB mRNA 表达增加，而所有脑区的 BDNF 表达增加，TrkB 表达减少。与对照组相比，CIA 大鼠中脑和海马中的羟色胺减少，而纹状体中的多巴胺减少。结论CIA 会导致神经炎症，同时出现细胞凋亡状态以及大脑中神经营养因子和单胺类物质的异常表达，这表明存在神经变性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Biology

自引率

0.00%

发文量