ABSTRACT

Background

Cerebral microbleeds (CMBs) are associated with a high risk for stroke . The present study determined whether long-term exposure to PM2.5 results in progressive worsening of CMBs and induction of systemic inflammation and microvascular oxidative stress.

Methods

Sixteen male Spontaneously hypertensive rats (SHR) and eight Wistar-Kyoto (WKY) rats were exposed to either filtered air or PM2.5 for 12 months. To detect CMBs, rats were imaged using a 7-T MRI. To determine systemic inflammation and oxidative stress, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), as well as reactive oxygen species (ROS), NADPH activity and its subunits p22/47/67phox & gp91phox were measured.

Results

During the exposure period, the mean daily concentration of PM2.5 was 59.2 ± 1.0 μg/m³. PM2.5 exposure significantly increased the incidence of CMBs compared to the PM2.5 (-) group (37.5% vs 12.5% incidence rate, p < 0.001). Animals exposed to PM2.5 also had significantly increased systolic blood pressures (SBPs) at 3 months (173 ± 5 vs 157 ± 5 mmHg, p < 0.05), 6 months (218 ± 6 vs 193 ± 7 mmHg, p < 0.01), 9 months (222 ± 6 vs 203 ± 8 mmHg, p < 0.05), and 12 months (231 ± 4 vs 207 ± 5 mmHg, p = 0.01). Additionally, there were significant elevations in IL-6, MCP-1, and TNF-α in the exposed group. Furthermore, PM2.5 significantly increased NOX activity and protein levels of gp91phox and p22/47/67phox.

Conclusion

In the SHR model, long-term exposure to PM2.5 worsened CMBs, increased SBPs, induced systemic inflammation and oxidative stress. Therefore, PM2.5 is potentially a controllable risk factor that promotes CMBs in certain patients, such as those with hypertension.

中文翻译：

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自发性高血压大鼠长期暴露在空气污染中可增加脑微出血

摘要

背景

脑微出血 (CMB) 与中风的高风险相关。本研究确定长期暴露于 PM2.5 是否会导致 CMB 进行性恶化以及诱导全身炎症和微血管氧化应激。

方法

16 只雄性自发性高血压大鼠 (SHR) 和 8 只 Wistar-Kyoto (WKY) 大鼠暴露于过滤空气或 PM2.5 中 12 个月。为了检测 CMB，使用 7-T MRI 对大鼠进行成像。为了确定全身炎症和氧化应激，白细胞介素 6 (IL-6)、肿瘤坏死因子-α (TNF-α)、单核细胞趋化蛋白 1 (MCP-1) 以及活性氧 (ROS)、NADPH活性及其亚基 p22/47/67phox & gp91phox 进行了测量。

结果

暴露期间，PM2.5日均浓度为59.2±1.0 μg/m ³。与 PM2.5 (-) 组相比，PM2.5 暴露显着增加了 CMB 的发生率（37.5% 对 12.5% 的发生率，p < 0.001）。暴露于 PM2.5 的动物在 3 个月（173 ± 5 vs 157 ± 5 mmHg，p < 0.05）、6 个月（218 ± 6 vs 193 ± 7 mmHg，p < 0.01）时收缩压 (SBP) 也显着升高, 9 个月 (222 ± 6 vs 203 ± 8 mmHg, p < 0.05) 和 12 个月 (231 ± 4 vs 207 ± 5 mmHg, p = 0.01)。此外，暴露组的 IL-6、MCP-1 和 TNF-α 显着升高。此外，PM2.5 显着增加了 gp91phox 和 p22/47/67phox 的 NOX 活性和蛋白质水平。

结论

在 SHR 模型中，长期暴露于 PM2.5 会恶化 CMB，增加 SBP，诱发全身炎症和氧化应激。因此，PM2.5 可能是促进某些患者（例如高血压患者）发生 CMB 的可控风险因素。