The cardiotoxicity of asthmatic rats after traffic-related PM2.5 and water-soluble components exposure mediated by endoplasmic reticulum stress and autophagy

• Published in: Environmental science and pollution research international Vol. 29; no. 33; pp. 50704 - 50716
• Main Authors: Tian, Jiayu, Shi, Hao, Wang, Xin, Wu, Hongyan, Wang, Caihong, Liu, Nannan, Wang, Dan, Shi, Dongxing, Zhang, Hongmei, Zhang, Zhihong
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.07.2022; Springer Nature B.V
• Subjects: Apoptosis; Aquatic Pollution; Asthma; Atmospheric Protection/Air Quality Control/Air Pollution; Autophagy; Cardiotoxicity; Cardiovascular system; Caspase-12; DNA nucleotidylexotransferase; Earth and Environmental Science; Ecotoxicology; Endoplasmic reticulum; Environment; Environmental Chemistry; Environmental Health; Environmental science; Gene expression; Molecular modelling; Ovalbumin; Particulate matter; Research Article; Respiratory system; Signal transduction; Transient receptor potential proteins; Waste Water Technology; Water chemistry; Water Management; Water Pollution Control; Traffic-related PM; Cardiotoxicity; Autophagy; Water-soluble components; Asthma; Endoplasmic reticulum stress; Apoptosis
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-022-19496-1

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.