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Ambient PM2.5-induced brain injury is associated with the activation of PI3K/AKT/FoxO1 pathway
Liying Song1, Kun Pan1, Xihao Du1
1Department of Environmental Health, School of Public Health and the Key Laboratory of Public Health Safety, Ministry of Education, Fudan University, Box 249, 130 Dong'an Road, Shanghai, 200032, China.
Abstract:
PM2.5-related neurological and mental diseases, such as cognitive impairment and stroke, tend to cause disability. Six-week-old male C57BL/6 mice were divided into 6 groups and exposed to concentrated PM2.5 or filtered air for 2, 4, and 6 months, respectively. The neurobehavioral changes of mice were tested. The weight of the whole brain and olfactory bulbs were recorded at the end of exposure, and the brain structure was observed by hematoxylin and eosin (HE) staining. Serum indicators, mRNA, and protein expressions were detected. The spatial learning memory ability was impaired, and the mice were more anxious after PM2.5 exposure. Relative brain weight decreased with age, and PM2.5 exposure exceeded the decrease of relative brain weight. Interestingly, superoxide dismutase (SOD) and albumin decreased in the PM2.5-exposed groups although neuronal morphology and other serum indicators did not show significant difference between PM and FA groups. Moreover, PM2.5 induced the increase of plasminogen at 2 months but recovered at 4 months and then increased at 6 months again. The results from protein expression and transcriptomic test demonstrated that PI3K/AKT/FoxO1 pathway might be activated after 6-month PM2.5 exposure in mice. Indicators albumin, the percentage of albumin over IgG (A/G value), and plasminogen were the main serous changes in mice after early-stage (2 months) and long-term (6 months) PM2.5 exposure. In addition, early-stage injury induced by PM2.5 might recover at later time point and display significant injury again with the exposure time. PM2.5 exposure-induced brain injury might be associated with the activation of PI3K/AKT/FoxO1 pathway.
Insights
Exposure to fine particulate matter (PM2.5) impairs spatial learning and increases anxiety in mice. Long-term PM2.5 exposure may activate the PI3K/AKT/FoxO1 pathway, suggesting a mechanism for neuroinflammation.
Area of Science:
- Environmental Health
- Neuroscience
- Toxicology
Background:
- Particulate matter (PM2.5) exposure is linked to neurological and mental health issues.
- Understanding the long-term effects of PM2.5 on brain health is crucial.
Purpose of the Study:
- To investigate the neurobehavioral and neurobiological effects of chronic PM2.5 exposure in mice.
- To identify potential molecular pathways involved in PM2.5-induced brain injury.
Main Methods:
- Mice were exposed to PM2.5 or filtered air for 2, 4, and 6 months.
- Neurobehavioral tests, brain weight measurements, histological analysis, and serum/molecular analyses were performed.
Main Results:
- PM2.5 exposure impaired spatial learning, increased anxiety, and reduced relative brain weight.
- Decreased superoxide dismutase (SOD) and albumin levels were observed.
- Plasminogen levels fluctuated, and the PI3K/AKT/FoxO1 pathway showed signs of activation after 6 months.
Conclusions:
- Chronic PM2.5 exposure induces neurobehavioral deficits and alters specific serum indicators.
- The PI3K/AKT/FoxO1 pathway may play a role in PM2.5-induced brain injury.
- Early-stage PM2.5-induced injury may show recovery followed by re-injury with prolonged exposure.
