PM2.5-induced inflammation and myocardial cell injury in rats.

Abstract

Numerous studies show association of particular matter (PM) in air pollution with cardiovascular dysfunction, and increased morbidity and mortality. The main mechanisms of this adverse effect involve increasing oxidative stress, inflammatory responses, and genotoxicity. Several recent studies investigated the ability of PM2.5 to cause myocardial injury in animal models using various methods, such as intratracheal instillation, intraperitoneal injection or tail vein injection. The purpose of this study is to explore the PM2.5-induced myocardial inflammatory reaction in rats through the new technology of multi-functional aerosol concentration and enrichment system. Thirty Wistar rats were divided into two groups, 15 in each group. In the exposure group, PM2.5 multi-functional aerosol concentration and enrichment system was used for PM2.5 online oral and nasal exposure (5 times a week, 4 hours exposure, for the duration of 3 months). Histopathological examination of the left ventricular myocardial tissue of both groups was done using hematoxylin and eosin (H&E) staining. Ultrastructural changes of the heart specimens were assessed using electron microscopy. The levels of CRP and ICAM-1 were detected by immunohistochemistry. Compared with the control group, myocardial tissue of the exposure group exhibited edema, widened myocardial space and infiltration of inflammatory cells. There was nuclear pyknosis, mitochondrial membrane and spinal fusion, rough endoplasmic reticulum expansion, degranulation and cell swelling in the exposed group. The area of CRP positive staining in the exposed group was 3.7-fold higher than that in the control group (p < 0.05), and the ICAM-1 positive staining area of the exposed group was 12-fold higher than that of the control group (p < 0.05). Prolonged exposure to PM2.5 inhalation promotes significant upregulation of ICAM-1 and CRP expression in myocardial tissues, ultrastructural alterations in myocardial cells, and influx of inflammatory cells.