Abstract:
Objective To investigate the mechanism of lung lesions caused by fine particulate matter PM2.5.
Methods Real-time PM2.5 collector was used to collect PM2.5. Wistar rats were fed on the systemic exposure system of PM2.5. Wistar rats were exposed to 4 hours daily for 9 months. PM2.5 experimental group and control group were set up. General structure of lung tissue and HE staining result were observed. T cell immune function, lung cell apoptosis, cell cycle and DNA index in Wistar rats were detected by flow cytometry. The expression levels of CEA, CA125 and SccAg in serum and lung lavage fluid of Wistar rats were detected by ELISA.
Results Lung tissues of experimental group were radiated from the periphery of the bronchus with dark, visible white spots and bubble like protrusions with irregular white ridges. HE staining results showed that lung tissues of experimental group were fibrotic, severe consolidation of lung, alveolar hyperemia and massive inflammaroty reactive hyperplasia. CD4/CD8 ratio in experimental group was significantly higher than that in control group(P < 0.05). The expression of CA125 in serum and lung lavage fluid was significantly higher than that in control group(P < 0.05). The apoptosis rate of lung tissues in experimental group was significantly lower than that in control group, but DNA index was significantly higher (P < 0.05).
Conclusion Long-term exposure to PM2.5 results in different degrees of nodules and a large range of inflammatory reaction in lung tissues.