Histopathological Evaluation of the Cerebrum in Neonatal Rats Following PM2.5 Particle Inhalation

The present study evaluated the effect of PM2.5 exposure on the cerebral tissue of neonatal rats. Twenty-four female Wistar albino rats were classified into three groups including control, Exposure1, and Exposure2 after mating and pregnancy. The control group used air with a clean standard condition, and the other two groups were exposed to gaseous pollutants and gaseous pollutants plus PM2.5 respectively for 40 days. The cerebral tissues were removed. Gene expression analysis was conducted for S100 and GFAP genes using quantitative real-time PCR and also western blot assay to indicate GFAP and S100 proteins level in the control, Exposure1, and Exposure2 groups. The histopathology, immunohistochemical staining, and oxidative stress (OS) activity were conducted for all groups. The results showed the significant expression of S100 and GFAP genes in Exposure1 and Exposure2 groups compared with the control group. The western blot analysis showed the significant increase of S100 and GFAP protein level in Exposure2 group. Based on the analysis of the involved enzymes in OS, superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) decreased, while malondialdehyde (MDA) increased in the Exposure1 and Exposure2 groups. According to the results of pathology and immunohistochemistry, severe tissue damage was observed in neonatal cerebral tissues in the Exposure2 group. These findings may help provide insight to identifying therapeutic targets for reducing human cerebral disorders caused by exposure to PM2.5 or other air pollutants.

Automated summary

This study evaluated the effects of PM2.5 exposure on neonatal rat cerebral tissue. The results showed significant increases in the expression of S100 and GFAP genes, as well as their associated proteins, in response to PM2.5 exposure. Pathological examination revealed severe tissue damage in the cerebral tissues of rats exposed to PM2.5. Changes in oxidative stress activity were also observed. These findings provide valuable insights for identifying therapeutic targets to reduce cerebral disorders caused by PM2.5 or other air pollutants.