<br>颗粒物暴露和慢性脑灌注不足促进雄性小鼠氧化应激并诱导神经元和少突胶质细胞凋亡,Journal of Neuroscience Research

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颗粒物暴露和慢性脑灌注不足促进雄性小鼠氧化应激并诱导神经元和少突胶质细胞凋亡
Journal of Neuroscience Research ( IF 2.9 ) Pub Date : 2022-12-04 , DOI: 10.1002/jnr.25153
Krista Lamorie-Foote _{1,

2} , Qinghai Liu ₁ , Kristina Shkirkova ₁ , Brandon Ge ₁ , Shannon He ₁ , Todd E Morgan ₃ , Wendy J Mack ₄ , Constantinos Sioutas ₅ , Caleb E Finch ₃ , William J Mack _{1,

2}

Affiliation

慢性脑灌注不足（CCH）可能会放大纳米颗粒物（nPM）的神经毒性，导致白质损伤。本研究描述了双侧颈动脉狭窄 (BCAS) 暴露后继发的 nPM（直径 ≤ 200 nm）和 CCH 对小鼠模型中神经元和白质损伤的联合影响。 nPM 在高速公路附近收集并重新雾化以进行暴露。十周大的 C57BL/6 雄性小鼠被随机分为四组：过滤空气 (FA)、nPM、FA + BCAS 和 nPM + BCAS。小鼠暴露于 FA 或 nPM 10 周。进行了 BCAS 手术。检查炎症、氧化应激和细胞凋亡的标志物。与 FA 相比，nPM + BCAS 暴露增加了大脑半球 TNFα 蛋白。与 FA 相比，nPM + BCAS 小鼠胼胝体和大脑皮层的 iNOS 和 HNE 免疫荧光增加。虽然单独暴露 nPM 不会减少皮质神经元细胞计数，但 nPM 会减少胼胝体少突胶质细胞计数。 nPM 暴露减少了胼胝体中成熟少突胶质细胞的数量，并增加了少突胶质细胞前体细胞的数量。与 FA 相比，nPM + BCAS 小鼠的皮质神经元 TUNEL 染色增加 200%，胼胝体少突胶质细胞 TUNEL 染色增加 700%。 nPM 和 BCAS 对皮质神经元 TUNEL 染色存在超加性相互作用（nPM + BCAS 的加性效应的 2.6 倍）。 nPM + BCAS 暴露增加了大脑皮层和胼胝体的细胞凋亡、神经炎症和氧化应激。 nPM + BCAS 暴露增加的神经元凋亡高于对每次暴露的单独反应。然而，胼胝体中的少突胶质细胞对 nPM + BCAS 暴露的联合神经毒性作用更敏感。

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Particulate matter exposure and chronic cerebral hypoperfusion promote oxidative stress and induce neuronal and oligodendrocyte apoptosis in male mice

Chronic cerebral hypoperfusion (CCH) may amplify the neurotoxicity of nanoscale particulate matter (nPM), resulting in white matter injury. This study characterized the joint effects of nPM (diameter ≤ 200 nm) and CCH secondary to bilateral carotid artery stenosis (BCAS) exposure on neuronal and white matter injury in a murine model. nPM was collected near a highway and re-aerosolized for exposure. Ten-week-old C57BL/6 male mice were randomized into four groups: filtered air (FA), nPM, FA + BCAS, and nPM + BCAS. Mice were exposed to FA or nPM for 10 weeks. BCAS surgeries were performed. Markers of inflammation, oxidative stress, and apoptosis were examined. nPM + BCAS exposure increased brain hemisphere TNFα protein compared to FA. iNOS and HNE immunofluorescence were increased in the corpus callosum and cerebral cortex of nPM + BCAS mice compared to FA. While nPM exposure alone did not decrease cortical neuronal cell count, nPM decreased corpus callosum oligodendrocyte cell count. nPM exposure decreased mature oligodendrocyte cell count and increased oligodendrocyte precursor cell count in the corpus callosum. nPM + BCAS mice exhibited a 200% increase in cortical neuronal TUNEL staining and a 700% increase in corpus callosum oligodendrocyte TUNEL staining compared to FA. There was a supra-additive interaction between nPM and BCAS on cortical neuronal TUNEL staining (2.6× the additive effects of nPM + BCAS). nPM + BCAS exposure increased apoptosis, neuroinflammation, and oxidative stress in the cerebral cortex and corpus callosum. nPM + BCAS exposure increased neuronal apoptosis above the separate responses to each exposure. However, oligodendrocytes in the corpus callosum demonstrated a greater susceptibility to the combined neurotoxic effects of nPM + BCAS exposure.

更新日期：2022-12-04

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