Ultrafine dust (PM2.5) is a fine particle with a diameter of less than 2.5 μm, mainly caused by exhaust fumes from fossil fuels, and has been known to affect respiratory and circulatory system diseases.
In the midst of this, it was found that ultrafine dust caused inflammation in the brain and aggravated the course of cerebral infarction. A research team at the Graduate School of Integrated Life Sciences at Hiroshima University in Japan announced in the International Journal of Toxicology (Particle and Fiber Toxicology) that they confirmed this through a cerebral infarction model mouse experiment.
According to a recent study, exposure to air pollutants such as ultrafine dust increases the hospitalization period of patients with cerebral infarction and increases the mortality rate within one year. However, the mechanism by which ultrafine dust exacerbates the course of cerebral infarction is unclear.
The research team administered 100 μg of physiological saline containing chemicals collected from a ventilation system filter in Beijing, China, for 7 days to cerebral infarction model mice, and then measured the activity of microglia (microglia), which are important for cognitive function.
As a result, it was found that microglia cells in the cerebral cortex became hypertrophic. It is said that when microglia run wild, the brain inflammatory response increases, which can lead to depression and Alzheimer’s.
Subsequently, when 10 μg/mL of ultrafine dust was administered to the neurons and microglia isolated from the mouse, an inflammatory response was observed in which only the microglia increased interleukin (IL)-6.
However, there was no change in serum cytokines, and microglia were affected in the central nervous system. In the cerebral infarction model mouse, the exercise capacity was also lowered.
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