Black phosphorus quantum dots induce myocardial inflammatory responses and metabolic disorders in mice.


Journal

Journal of environmental sciences (China)
ISSN: 1001-0742
Titre abrégé: J Environ Sci (China)
Pays: Netherlands
ID NLM: 100967627

Informations de publication

Date de publication:
Mar 2024
Historique:
received: 01 09 2022
revised: 30 12 2022
accepted: 03 01 2023
medline: 20 11 2023
pubmed: 19 11 2023
entrez: 18 11 2023
Statut: ppublish

Résumé

As an ultrasmall derivative of black phosphorus (BP) sheets, BP quantum dots (BP-QDs) have been effectively used in many fields. Currently, information on the cardiotoxicity induced by BP-QDs remains limited. We aimed to evaluate BP-QD-induced cardiac toxicity in mice. Histopathological examination of heart tissue sections was performed. Transcriptome sequencing, real-time quantitative PCR (RT‒qPCR), western blotting, and enzyme-linked immunosorbent assay (ELISA) assays were used to detect the mRNA and/or protein expression of proinflammatory cytokines, nuclear factor kappa B (NF-κB), phosphatidylinositol 3 kinase-protein kinase B (PI3K-AKT), peroxisome proliferator-activated receptor gamma (PPARγ), and glucose/lipid metabolism pathway-related genes. We found that heart weight and heart/body weight index (HBI) were significantly reduced in mice after intragastric administration of 0.1 or 1 mg/kg BP-QDs for 28 days. In addition, obvious inflammatory cell infiltration and increased cardiomyocyte diameter were observed in the BP-QD-treated groups. Altered expression of proinflammatory cytokines and genes related to the NF-κB signaling pathway further confirmed that BP-QD exposure induced inflammatory responses. In addition, BP-QD treatment also affected the PI3K-AKT, PPARγ, thermogenesis, oxidative phosphorylation, and cardiac muscle contraction signaling pathways. The expression of genes related to glucose/lipid metabolism signaling pathways was dramatically affected by BP-QD exposure, and the effect was primarily mediated by the PPAR signaling pathway. Our study provides new insights into the toxicity of BP-QDs to human health.

Identifiants

pubmed: 37980037
pii: S1001-0742(23)00007-4
doi: 10.1016/j.jes.2023.01.004
pii:
doi:

Substances chimiques

Proto-Oncogene Proteins c-akt EC 2.7.11.1
NF-kappa B 0
PPAR gamma 0
Phosphatidylinositol 3-Kinases EC 2.7.1.-
Cytokines 0
Glucose IY9XDZ35W2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

53-64

Informations de copyright

Copyright © 2023. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

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 article.

Auteurs

Chao Shen (C)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China.

Xiaoyan Ding (X)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China.

Jinpeng Ruan (J)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China.

Fengkai Ruan (F)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China.

Weiping Hu (W)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China.

Jiyi Huang (J)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China.

Chengyong He (C)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China.

Yi Yu (Y)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China. Electronic address: yuyicn@126.com.

Zhenghong Zuo (Z)

Department of Nephrology, State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Sciences, Fujian Clinical Research Center for Chronic Glomerular Disease, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China. Electronic address: zuozhenghong@xmu.edu.cn.

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Classifications MeSH