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Polystyrene Microplastics Induce Injury to the Vascular Endothelial Through NLRP3-Mediated Pyroptosis
Chuanyi Huo1, Ying Zhu1, Xiaoqi Fang1
1Department of Occupational and Environmental Health, School of Public Health, Jilin University, Changchun, China.
Abstract:
The health risks associated with microplastics have attracted widespread attention. Polystyrene microplastics (PS-MPs) can induce damage to cardiac tissue, while pyroptosis-mediated injury to the vascular endothelial plays a vital role in the pathogenesis of cardiovascular diseases. The study intended to explore the role and mechanism of NLR family pyrin domain containing 3 (NLRP3) mediated pyroptosis in PS-MPs causing the injury of vascular endothelial cells. In vivo, Wistar rats were exposed to 0.5, 5, and 50 mg/kg/d 0.5 μm PS-MPs. In vitro, the human vascular endothelial cells (HUVECs) were used for mechanistic studies. siRNA was used for silencing the NILRP3 gene. H&E staining and flow cytometry were performed to examine the vascular injury and cell membrane damage. The oxidative stress was detected by flow cytometry, immunofluorescence, and corresponding kits. ELISA were used to measure the levels of inflammatory factors. Real-time PCR and western blot were used to measure the expression of pyroptosis signaling pathway. In rats, PS-MPs could cause vascular damage, oxidative stress, and inflammatory response, and activated the pyroptosis signaling pathway. HUVECs exposure to PS-MPs, the vitality decreased in a dose-dependent manner, ROS and MDA were significantly increased while SOD was decreased. PS-MPs induced the onset of pyroptosis signaling pathway in HUVECs. Cell membrane damage and the levels of IL-Iβ and IL-18 in HUVECs significantly increased, those are symbols for the development of pyroptosis. Inhibition of NLRP3-mediated pyroptosis effectively protected HUVECs from PS-MPs-induced damage. Pyroptosis played a vital role in controlling the vascular endothelial injury caused by PS-MPs.
Insights
Polystyrene microplastics (PS-MPs) cause vascular endothelial cell injury via NLRP3-mediated pyroptosis. Inhibiting this pathway protected cells, highlighting pyroptosis
Area of Science:
- Environmental Toxicology
- Cardiovascular Research
- Cellular Biology
Background:
- Microplastic pollution, particularly polystyrene microplastics (PS-MPs), poses significant health risks.
- Vascular endothelial injury, driven by pyroptosis, is crucial in cardiovascular disease development.
- The specific role of NLRP3-mediated pyroptosis in PS-MP-induced vascular damage requires elucidation.
Purpose of the Study:
- To investigate the mechanism of NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated pyroptosis in PS-MP-induced vascular endothelial cell injury.
- To assess the impact of PS-MPs on vascular integrity, oxidative stress, and inflammatory responses in vivo and in vitro.
Main Methods:
- In vivo studies using Wistar rats exposed to varying doses of PS-MPs.
- In vitro studies utilizing human vascular endothelial cells (HUVECs) with NLRP3 gene silencing (siRNA).
- Assays included H&E staining, flow cytometry, ELISA, real-time PCR, and western blot to evaluate vascular injury, cell damage, oxidative stress, inflammation, and pyroptosis pathway activation.
Main Results:
- PS-MPs induced vascular damage, oxidative stress, inflammation, and activated the pyroptosis pathway in rats.
- In HUVECs, PS-MPs decreased viability, increased reactive oxygen species (ROS) and malondialdehyde (MDA), and decreased superoxide dismutase (SOD) in a dose-dependent manner.
- PS-MPs triggered pyroptosis in HUVECs, evidenced by increased cell membrane damage and elevated IL-1β and IL-18 levels; NLRP3 inhibition mitigated these effects.
Conclusions:
- Pyroptosis plays a critical role in PS-MP-induced vascular endothelial cell injury.
- NLRP3 inflammasome activation is a key mechanism underlying PS-MP-induced endothelial damage.
- Targeting NLRP3-mediated pyroptosis may offer a therapeutic strategy against microplastic-related cardiovascular risks.
