Davidson Honors College, University of Montana, 32 Campus Drive, 287 Skaggs Bldg, Missoula, MT 59812, USA.
Int J Toxicol. 2010 Dec;29(6):604-15. doi: 10.1177/1091581810383587. Epub 2010 Oct 28.
Mexico City (MC) residents exposed to fine particulate matter and endotoxin exhibit inflammation of the olfactory bulb, substantia nigra, and vagus nerve. The goal of this study was to model these endpoints in mice and examine the neuroprotective effects of chocolate. Mice exposed to MC air received no treatment or oral dark chocolate and were compared to clean-air mice either untreated or treated intraperitoneally with endotoxin. Cyclooxygenase-2 (COX-2), interleukin 1 beta (IL-1β), and CD14 messenger RNA (mRNA) were quantified after 4, 8, and 16 months of exposure in target brain regions. After 16 months of exposure, the dorsal vagal complex (DVC) exhibited significant inflammation in endotoxin-treated and MC mice (COX-2 and IL-1β P<.001). Mexico City mice had olfactory bulb upregulation of CD14 (P=.002) and significant DVC imbalance in genes for antioxidant defenses, apoptosis, and neurodegeneration. These findings demonstrate sustained DVC inflammation in mice exposed to MC air, which is mitigated by chocolate administration.
墨西哥城(MC)居民暴露于细颗粒物和内毒素会导致嗅球、黑质和迷走神经发炎。本研究的目的是在小鼠中模拟这些终点,并研究巧克力的神经保护作用。暴露于 MC 空气的小鼠未接受任何治疗或口服黑巧克力,并与未暴露于清洁空气或腹腔内接受内毒素治疗的小鼠进行比较。在暴露 4、8 和 16 个月后,在目标脑区定量检测环氧化酶-2(COX-2)、白细胞介素 1β(IL-1β)和 CD14 信使 RNA(mRNA)。暴露 16 个月后,迷走神经背核复合体(DVC)在接受内毒素和 MC 处理的小鼠中表现出明显的炎症(COX-2 和 IL-1β P<.001)。MC 暴露的小鼠嗅球 CD14 上调(P=.002),抗氧化防御、细胞凋亡和神经退行性变相关基因的 DVC 失衡显著。这些发现表明,暴露于 MC 空气中的小鼠持续存在 DVC 炎症,而巧克力的摄入可减轻这种炎症。