Hiroshima [Japan], May 10 (ANI): The specific mechanism through which air pollution affects the prognosis of ischemic stroke, or stroke caused by diminished blood supply to the brain, is uncertain. A group of researchers recently undertook a study to see if increased inflammation in the brain, often known as neuroinflammation, is to blame.
The team published their findings in the February 16, 2023 issue of Particle and Fibre Toxicology.
Mice treated intranasally to Beijing, China, urban aerosols for one week showed greater neuroinflammation and worsened mobility dysfunction following ischemic stroke compared to control mice not exposed to air pollution. Furthermore, this impact was not found in urban-aerosol-treated mice missing a receptor for polycyclic aromatic hydrocarbons (PAH), which are compounds generated by the combustion of fossil fuels, wood, waste, and tobacco. This shows that PAHs are implicated in both neuroinflammation and greater mobility dysfunction in ischemic stroke caused by air pollution exposure.
“We designed this study to determine the effects of air pollution on disorders in the central nervous system,” said Yasuhiro Ishihara, senior author of the research paper and professor in the Graduate School of Integrated Sciences for Life at Hiroshima University. “Our narrower focus was to determine whether or not the prognosis of ischemic stroke was affected by air pollution,” said Ishihara.
The group went one step further by identifying specific components of air pollution that may directly contribute to lower prognoses in ischemic stroke.
They found evidence that intranasal exposure to air pollution from Beijing, China, increased neuroinflammation after ischemic stroke in mice through activation of microglial cells, which are immune cells found in the brain. Movement disorder was also negatively impacted in ischemic stroke mice exposed to the same air pollution. A second set of experiments replacing Beijing air pollution with PM2.5 (tiny, aerosolized particles of air pollution that are 2.5 microbes in width or less) from Yokohama, Japan demonstrated similar results, suggesting the PM2.5 fraction of urban air pollution contains the chemical responsible for increased neuroinflammation and decreased ischemic stroke prognosis.
In order to identify chemicals in air pollution responsible for decreased ischemic stroke prognosis, the research team used a mouse that lacked the aryl hydrocarbon receptor, a receptor that is activated by the presence of PAHs, to determine whether or not exposure to the Beijing air pollution would have the similar effect on mice without working aryl hydrocarbon receptors. Mice lacking the aryl hydrocarbon receptor demonstrated lower microglial cell activation and movement disorder compared to normal mice, suggesting that the PAHs present in Beijing air pollution are responsible for at least some of the neuroinflammation and lower prognosis seen in ischemic stroke mice exposed to air pollution. (ANI)
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