4.7 Article

The impact of polystyrene microplastics on cardiomyocytes pyroptosis through NLRP3/Caspase-1 signaling pathway and oxidative stress in Wistar rats

Journal

ENVIRONMENTAL TOXICOLOGY
Volume 36, Issue 5, Pages 935-944

Publisher

WILEY
DOI: 10.1002/tox.23095

Keywords

cardiotoxicity; inflammatory stimuli; microplastics; oxidative stress; pyroptosis

Funding

  1. National Natural Science Foundation of China [81903362]

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The study revealed that exposure to microplastics can damage cardiac structure and function in Wistar rats, leading to oxidative stress, pyroptosis, apoptosis, and activation of inflammasomes in cardiac tissue. These findings suggest that pyroptosis plays a crucial role in microplastic-induced cardiotoxicity and may contribute to understanding the mechanisms of cardiac dysfunction caused by microplastics.
The extensive existing of microplastics (MPs) in the ecosystem have increased considerable attention concerning their potential adverse effects, the toxicities and the underlying mechanism of MPs are still scarce. To explore the effect of MPs on cardiac tissue in Wistar rats and unravel the mechanism of pyroptosis and oxidative stress in the process of cardiomyocytes injury, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.5 mm PS MPs at 0.5, 5 and 50 mg/L for 90 days. Results revealed that MPs could damage cardiac structure and function with impaired mitochondria integrity, as well as increased levels of creatine kinase-MB and cardiac troponinI (cTnI). Moreover, MPs administration triggered oxidative stress as indicated by increased levels of malondialdehyde and decreased activity of superoxide dismutase, glutathione peroxidase and catalase. Treatment with MPs resulted in apoptosis and pyroptosis as evidenced by increasing expressions of interleukin (IL)-1 beta, IL-18. Additionally, MPs were shown to induce the NOD-like receptor protein 3 inflammasomes activation in cardiac tissue, enabling activation of Caspase-1-dependent signaling pathway induced by inflammatory stimuli resulting from oxidative stress. In summary, these results illustrated that pyroptosis played a vital role in polystyrene MPs-induced cardiotoxicity, which might be helpful to understand the mechanism of cardiac dysfunction and induced by MPs.

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