Premium
NLRP3 inflammasome activation is associated with PM 2.5 ‐induced cardiac functional and pathological injury in mice
Author(s) -
Duan Shuyin,
Wang Na,
Huang Li,
Zhao Ying,
Shao Hua,
Jin Yuefei,
Zhang Ruiqin,
Li Chunyang,
Wu Weidong,
Wang Jing,
Feng Feifei
Publication year - 2019
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22825
Subject(s) - inflammasome , inflammation , pathological , fibrosis , caspase 1 , cardiac fibrosis , downregulation and upregulation , medicine , chemokine , endocrinology , chemistry , pathology , biochemistry , gene
Growing evidences indicate that inflammation induced by PM 2.5 exposure has been considered as a major driving force for the development of cardiovascular diseases. However, the mechanisms underlying PM 2.5 ‐induced cardiac injury remain unclear. This study aims to investigate the role of NLRP3 inflammasome in PM 2.5 ‐induced cardiac functional and pathological injury in mice. In this study, BALB/c mice were intratracheally instilled with PM 2.5 suspension (4.0 mg/kg BW) for 5 days to set up a cardiac injury model, which was evaluated by electrocardiogram monitoring, HE and Masson staining. Then, the effects of PM 2.5 on the expression of α‐SMA, NLRP3, IL‐1β, and IL‐18 proteins and the activation of caspase‐1 and IL‐1β were investigated. The results showed that PM 2.5 exposure induced characteristic abnormal ECG changes such as the abnormality of heart rhythm, tachycardia, and T‐wave reduction. Inflammatory cell infiltration and fibrosis were observed in the heart tissues of PM 2.5 ‐exposed mice. Meanwhile, PM 2.5 exposure increased the expression of α‐SMA. And, NLRP3 activation‐associated proteins of NLRP3, IL‐1β, IL‐18, Cleaved caspase‐1 p10, and Cleaved IL‐1β were upregulated in heart tissue of PM 2.5 ‐induced mice. In summary, PM 2.5 exposure could induce cardiac functional and pathological injury, which may be associated with the activation of NLRP3 inflammasome.