动物造模 z-bio 2022-07-11 431

　　Objective: To study the effects of chronic PM2.5 exposure on pneumonia and NLRP3 inflammasome activity in mice, and to provide new targets for the prevention and treatment of PM2.5-induced lung injury.

　　Methods: Male C57BL/6J mice were infused with PM2.5 by different doses of tracheal instillation, with a dose of 2,10 mg/(kg∙bw), and the mice in the control group were instilled with normal saline. Mice were instilled 20 times in a row After exposure every 3 days, blood and lung tissue were collected. Three groups of mice were counted for blood cells; the level of macrophages in lung tissue was detected by immunofluorescence staining; the interleukin (IL) in lung tissue was determined by kit )-1β, IL-18 levels and caspase-1 activity; real-time quantitative PCR was used to detect NLRP3 inflammasome-related mRNA expression levels in lung tissue.

　　Results: Both doses of PM2.5 exposure could significantly reduce the percentage of monocytes (P<0.01) and increase the percentage of neutrophils (P<0.01); lead to pneumonia; increase the activity of caspase-1 in lung tissue (P<0.01). <0.01) and the mRNA expression of NLRP3 and ASC (P<0.01). Compared with the control group, the levels of IL-1β and IL-18 in the lung tissue of mice in the two dose groups were significantly increased (P<0.01).

　　Conclusion: Chronic PM2.5 exposure may lead to pneumonia by activating NLRP3 inflammasome in lung tissue.