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Tytuł:
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NLRP3 inflammasome-mediated endothelial cells pyroptosis is involved in decabromodiphenyl ethane-induced vascular endothelial injury.
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Autorzy:
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Zheng D; School of Public Health and Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China.
Shi Z; School of Public Health and Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China.
Yang M; School of Public Health and Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China.
Liang B; School of Public Health and Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China.
Zhou X; School of Public Health and Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China.
Jing L; School of Public Health and Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China. Electronic address: .
Sun Z; School of Public Health and Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China.
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Źródło:
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Chemosphere [Chemosphere] 2021 Mar; Vol. 267, pp. 128867. Date of Electronic Publication: 2020 Nov 05.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Publication: Oxford : Elsevier Science Ltd
Original Publication: Oxford, New York, : Pergamon Press.
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MeSH Terms:
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Inflammasomes*
Pyroptosis*
Animals ; Bromobenzenes ; Endothelial Cells ; Endothelium ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Proteins ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species
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Contributed Indexing:
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Keywords: Caspase-1; Decabromodiphenyl ethane; NLRP3; Pyroptosis; Vascular endothelial
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Substance Nomenclature:
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0 (Bromobenzenes)
0 (Inflammasomes)
0 (Interleukin-1beta)
0 (NLR Family, Pyrin Domain-Containing 3 Protein)
0 (NLR Proteins)
0 (Nlrp3 protein, rat)
0 (Reactive Oxygen Species)
0 (decabromodiphenyl ethane)
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Entry Date(s):
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Date Created: 20201114 Date Completed: 20210121 Latest Revision: 20220531
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Update Code:
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20240105
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DOI:
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10.1016/j.chemosphere.2020.128867
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PMID:
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33187650
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Decabromodiphenyl ethane (DBDPE) is a novel environmental pollutant that has attracted growing attention. Previous studies have indicated that DBDPE could induce vascular endothelial injury and cardiovascular damage, but the underlying mechanisms are not well understood. This study was designed to examine the mechanisms of DBDPE induces vascular endothelial injury. In vivo, Sprague-Dawley rats were administered with 0, 5, 50, 500 mg/kg bw/day of DBDPE via gavage for 28 days. Results showed that DBDPE could damage abdominal aortas morphological and ultrastructural structure and increase the protein levels of interleukin 1β (IL-1β) and interleukin 18 (IL-18) of the abdominal aortas. Moreover, DBDPE induced NLRP3 inflammasome activation and activated caspase-1 in abdominal aorta endothelium of rats. In vitro, human vascular endothelial cells (HAECs) were treated with different concentrations of DBDPE (0, 6.25, 12.5, 25, 50, and 100 μM). DBDPE not only induced cytotoxicity and reactive oxygen species (ROS) generation in HAECs but also caused HAECs pyroptosis, which was evidenced by the elevated expression of Nod-like receptor protein -3 (NLRP3), ASC, and caspase-1 in DBDPE-treated group. To further elucidate the effects of NLRP3 inflammasome on DBDPE-induced HAECs pyroptosis, we constructed NLRP3 knockdown HAECs by lentivirus-mediated short hairpin RNA (shRNA). And the results showed that NLRP3 knockdown downregulated DBDPE-induced increases of caspase-1 activity and caspase-1, ASC and NLRP3 mRNA and protein expression levels. Accordingly, our data suggested that DBDPE may damage vascular endothelium by NLRP3 inflammasome-mediated endothelial cells pyroptosis.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2020 Elsevier Ltd. All rights reserved.)
