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银河系宇宙射线粒子暴露不会增加大鼠小胶质细胞体外炎症或氧化应激标志物的蛋白水平。

Galactic Cosmic Ray Particle Exposure Does Not Increase Protein Levels of Inflammation or Oxidative Stress Markers in Rat Microglial Cells In Vitro.

机构信息

USDA-ARS, Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.

Department of Psychology, University of Maryland, Baltimore County (UMBC), Baltimore, MD 21250, USA.

出版信息

Int J Mol Sci. 2024 May 29;25(11):5923. doi: 10.3390/ijms25115923.

DOI:10.3390/ijms25115923
PMID:38892109
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11172496/
Abstract

Astronauts on exploratory missions will be exposed to galactic cosmic rays (GCR), which can induce neuroinflammation and oxidative stress (OS) and may increase the risk of neurodegenerative disease. As key regulators of inflammation and OS in the CNS, microglial cells may be involved in GCR-induced deficits, and therefore could be a target for neuroprotection. This study assessed the effects of exposure to helium (He) and iron (Fe) particles on inflammation and OS in microglia in vitro, to establish a model for testing countermeasure efficacy. Rat microglia were exposed to a single dose of 20 cGy (300 MeV/n) He or 2 Gy Fe (600 MeV/n), while the control cells were not exposed (0 cGy). Immediately following irradiation, fresh media was applied to the cells, and biomarkers of inflammation (cyclooxygenase-2 [COX-2], nitric oxide synthase [iNOS], phosphorylated IκB-α [pIκB-α], tumor necrosis factor-α [TNFα], and nitrite [NO]) and OS (NADPH oxidase [NOX2]) were assessed 24 h later using standard immunochemical techniques. Results showed that radiation did not increase levels of NO or protein levels of COX-2, iNOS, pIκB-α, TNFα, or NOX2 compared to non-irradiated control conditions in microglial cells ( > 0.05). Therefore, microglia in isolation may not be the primary cause of neuroinflammation and OS following exposures to helium or iron GCR particles.

摘要

宇航员在探索任务中会暴露在银河宇宙射线(GCR)下,这可能会引起神经炎症和氧化应激(OS),并增加神经退行性疾病的风险。作为中枢神经系统中炎症和 OS 的关键调节剂,小胶质细胞可能参与了 GCR 诱导的损伤,因此可能成为神经保护的靶点。本研究评估了暴露于氦(He)和铁(Fe)颗粒对体外小胶质细胞炎症和 OS 的影响,为测试对策功效建立了模型。用 20 cGy(300 MeV/n)He 或 2 Gy Fe(600 MeV/n)对大鼠小胶质细胞进行单次照射,而对照细胞不进行照射(0 cGy)。照射后立即向细胞中添加新鲜培养基,24 小时后使用标准免疫化学技术评估炎症标志物(环氧化酶-2 [COX-2]、一氧化氮合酶 [iNOS]、磷酸化 IκB-α [pIκB-α]、肿瘤坏死因子-α [TNFα]和亚硝酸盐 [NO])和 OS(NADPH 氧化酶 [NOX2])。结果表明,与未照射对照条件相比,辐射不会增加小胶质细胞中 NO 或 COX-2、iNOS、pIκB-α、TNFα 或 NOX2 的蛋白水平(>0.05)。因此,在单独暴露于氦或铁 GCR 颗粒后,小胶质细胞可能不是神经炎症和 OS 的主要原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be0b/11172496/b0522bf0bb75/ijms-25-05923-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be0b/11172496/ab08b49c7c23/ijms-25-05923-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be0b/11172496/20bd7f2b1c5c/ijms-25-05923-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be0b/11172496/b0522bf0bb75/ijms-25-05923-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be0b/11172496/ab08b49c7c23/ijms-25-05923-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be0b/11172496/20bd7f2b1c5c/ijms-25-05923-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be0b/11172496/b0522bf0bb75/ijms-25-05923-g003.jpg

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本文引用的文献

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2
Blueberry treatment administered before and/or after lipopolysaccharide stimulation attenuates inflammation and oxidative stress in rat microglial cells.蓝莓处理在脂多糖刺激之前和/或之后给予可减轻大鼠小胶质细胞中的炎症和氧化应激。
Nutr Neurosci. 2023 Feb;26(2):127-137. doi: 10.1080/1028415X.2021.2020404. Epub 2022 Jan 4.
3
Effects of partial- or whole-body exposures to Fe particles on brain function and cognitive performance in rats.
局部或全身暴露于 Fe 颗粒对大鼠脑功能和认知表现的影响。
Life Sci Space Res (Amst). 2020 Nov;27:56-63. doi: 10.1016/j.lssr.2020.07.006. Epub 2020 Jul 24.
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Effects of Six Sequential Charged Particle Beams on Behavioral and Cognitive Performance in B6D2F1 Female and Male Mice.六次连续带电粒子束对B6D2F1雌性和雄性小鼠行为及认知能力的影响
Front Physiol. 2020 Aug 28;11:959. doi: 10.3389/fphys.2020.00959. eCollection 2020.
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Mitigation of helium irradiation-induced brain injury by microglia depletion.小胶质细胞耗竭减轻氦离子辐照诱导的脑损伤。
J Neuroinflammation. 2020 May 19;17(1):159. doi: 10.1186/s12974-020-01790-9.
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Space-like Fe irradiation manifests mild, early sex-specific behavioral and neuropathological changes in wildtype and Alzheimer's-like transgenic mice.类太空辐射导致野生型和阿尔茨海默病样转基因小鼠出现轻微的、早期性别特异性行为和神经病理学改变。
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