Fine particulate matter 2.5 (PM), one of the main components of air pollutants, seriously threatens human health. Possible neuronal dysfunction induced by PM has received extensive attention. However, there is little evidence for the specific biochemical mechanism of neuronal injury induced by PM. Moreover, the pathway for PM transport from peripheral circulation to the central nervous system (CNS) is still unclear. In the current work, C57BL/6 mice were chronically exposed to ambient PM for 3, 6, 9, and 12 months. Exposure to ambient PM resulted in a significant reduction of cognitive ability in mice by Morris water maze test. PM exposure induced a neuroinflammatory reaction after cognitive impairment, while inflammation in the hypothalamus and olfactory bulb tissue occurred earlier. The expression levels of integrity tight junction proteins in the blood-brain barrier (BBB) were reduced by PM exposure. Pulmonary inflammation occurred much earlier and diminished at later stage of PM exposure. The results indicated that chronic exposure to ambient PM led to cognitive decline in mice; CNS dysfunction may be due to neuroinflammatory reactions; the reduced integrity of the BBB allowed the influence of pulmonary inflammation to neuronal alterations. The work may provide promising therapeutic or preventive targets for air pollution-induced neurodegenerative disease.
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| http://dx.doi.org/10.1016/j.toxlet.2020.06.014 | DOI Listing |
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