The cardiotoxicity of asthmatic rats after traffic-related PM2.5 and water-soluble components exposure mediated by endoplasmic reticulum stress and autophagy
2022
Tian, Jiayu | Shi, Hao | Wang, Xin | Zhending, | Wang, Caihong | Liu, Nannan | Wang, Dan | Shi, Dongxing | Zhang, Hongmei | Zhang, Zhihong
Fine particulate matter (PM₂.₅) 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 PM₂.₅ (TRPM₂.₅) 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 TRPM₂.₅ and WSC every 3 days in total of eight times. Significant myocardial pathological changes were observed in the TRPM₂.₅ and WSC group by hematoxylin-eosin (HE) staining. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) results demonstrated TRPM₂.₅ 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, TRPM₂.₅ and WSC activated autophagy via upregulation of LC3 and p62 gene and protein expression. In conclusion, TRPM₂.₅ and WSC may aggravate heart injury in asthmatic rats, possibly through the activation of ERS and autophagy signaling pathway.
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