The cardiotoxicity of asthmatic rats after traffic-related PM 2.5 and water-soluble components exposure mediated by endoplasmic reticulum stress and autophagy

Fine particulate matter (PM 2.5 ) is closely related to cardiopulmonary diseases; it is known that the respiratory system is related to the cardiovascular system. This study aimed to investigate the toxic effects of traffic-related PM 2.5 (TRPM 2.5 ) and water-soluble components (WSC) on hearts of asthmatic rats and explore potential molecular mechanisms. Here, ovalbumin (OVA)-sensitized asthmatic rats were intratracheally instilled with TRPM 2.5 and WSC every 3 days in total of eight times. Significant myocardial pathological changes were observed in the TRPM 2.5 and WSC group by hematoxylin-eosin (HE) staining. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) results demonstrated TRPM 2.5 and WSC aggravated apoptosis of myocardial cells, which may be triggered by endoplasmic reticulum stress (ERS), as manifested by elevated GRP78, CHOP, and caspase-12. Likewise, TRPM 2.5 and WSC activated autophagy via upregulation of LC3 and p62 gene and protein expression. In conclusion, TRPM 2.5 and WSC may aggravate heart injury in asthmatic rats, possibly through the activation of ERS and autophagy signaling pathway.