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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.

Both the epidemiological and animal experimental studies have reported the association between PM2.5 and respiratory, cardiovascular, and metabolic diseases. However, the study linking PM2.5 and hepatic injury is few, and the relative mechanism has not been fully elucidated. Thirty-two 6-week-old male C57BL/6 mice were exposed to filtered air (FA) or concentrated PM2.5 for 12 weeks using Shanghai Meteorological and Environmental Animal Exposure System (“Shanghai-METAS”), respectively. At week 11, the mice began to be treated with intraperitoneal injection of normal 0.9% saline or AMPK activator (AICAR). The mRNA levels of IL-6 and TNF-α, and protein expressions of AMPK, GLUT4, NF-κB, p38MAPK, ERK, and JNK in the liver and UCP-1 in brown adipose tissue (BAT) were measured. Meanwhile, histopathological examination both in the liver and BAT was performed to evaluate the histopathological changes. PM2.5 exposure induced steatosis, hepatocyte ballooning, lobular and portal inflammation in the liver, and the brown adipocyte swelling in BAT. The results found that PM mice displayed higher IL-6, TNF-α, NF-κB, and JNK expression and lower AMPK, GLUT4, and UCP-1 when compared with FA mice. The AICAR injection upregulated the expressions of GLUT4 in the liver of PM-AIC mice when compared with the PM mice. However, there were no significant effects of AICAR on histopathological condition. The current study showed that ambient PM2.5 exposure might induce the hepatic injury along with the lipid metabolism disorder in BAT. AMPK activation can ameliorate most of the harmful effects and might become the potential target for treating PM2.5-induced hepatic injury.

Substantial epidemiological and experimental studies have shown that ambient fine particulate matter (PM2.5) exposure can lead to myocardial damage in human and animal through the mechanism of inflammation and oxidative stress. The purpose of the current study was to investigate whether selenium yeast (SeY) supplementation could prevent cardiovascular injury caused by PM2.5 in rats. Fifty-six Sprague-Dawley rats were randomly divided into seven groups: saline control group; solvent control group, low-, middle-, and high-dose Se pretreatment groups, PM2.5 exposure group, and high-dose Se control group. The rats were pretreated with different concentration of dietary SeY for 28 days, then were exposed to PM2.5 by intratracheal instillation every other day, a total of three times. The levels of inflammatory markers (tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), soluble intercellular adhesion molecule-1 (sICAM-1), and oxidative responses-related indicators total antioxidant capacity (T-AOC), total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were measured in blood and myocardium of the left ventricle. The results showed that although PM2.5 caused a decrease of T-AOC, T-AOD, and GSH-Px and increase of MDA and sICM-1, pretreatment with SeY induced a dose-dependent increase in these anti-oxidative indicators and a decrease in oxidative indicators. In addition, the levels of TNF-α and IL-1β in Se pretreatment groups were significantly lower than that in PM2.5 exposure group. The results indicated that Se supplementation could effectively prevent cardiovascular inflammation and oxidative stress induced by PM2.5. The results also indicated that the nutritional supplementation might be an effective way to protecting people’s health from air pollution.