Mitochondria-Modulating Porous Se@Si[O.sub.2] Nanoparticles Provide Resistance to Oxidative Injury in Airway Epithelial Cells: Implications for Acute Lung Injury

Background: Mitochondrial dysfunction played a vital role in the pathogenesis of various diseases, including acute lung injury (ALI). However, few strategies targeting mitochondria were developed in treating ALI. Recently, we fabricated a porous Se@Si[O.sub.2] nanoparticles (NPs) with antioxidant pr...

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Published inInternational journal of nanomedicine p. 2287
Main Authors Wang, Muyun, Wang, Kun, Deng, Guoying, Liu, Xijian, Wu, Xiaodong, Hu, Haiyang, Zhang, Yanbei, Gao, Wei, Li, Qiang
Format Journal Article
LanguageEnglish
Published Dove Medical Press Limited 31.05.2020
Subjects
Antioxidants (Nutrients)
B cells
Diseases
Electron microscopy
Gene expression
Genes
Inflammation
Lung diseases
Medical research
Microscopy
Mitogens
Nanoparticles
Oxidative stress
Povidone
RNA
United Kingdom
China
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Summary:Background: Mitochondrial dysfunction played a vital role in the pathogenesis of various diseases, including acute lung injury (ALI). However, few strategies targeting mitochondria were developed in treating ALI. Recently, we fabricated a porous Se@Si[O.sub.2] nanoparticles (NPs) with antioxidant properties. Methods: The protective effect of Se@Si[O.sub.2] NPs was assessed using confocal imaging, immunoblotting, RNA-seq, mitochondrial respiratory chain (MRC) activity assay, and transmission electron microscopy (TEM) in airway epithelial cell line (Beas-2B). The in vivo efficacy of Se@Si[O.sub.2] NPs was evaluated in a lipopolysaccharide (LPS)-induced ALI mouse model. Results: This study demonstrated that Se@Si[O.sub.2] NPs significantly increased the resistance of airway epithelial cells under oxidative injury and shifted lipopolysaccharide-induced gene expression profile closer to the untreated controls. The cytoprotection of Se@Si[O.sub.2] was found to be achieved by maintaining mitochondrial function, activity, and dynamics. In an animal model of ALI, pretreated with the NPs improved mitochondrial dysfunction, thus reducing inflammatory responses and diffuse damage in lung tissues. Additionally, RNA-seq analysis provided evidence for the broad modulatory activity of our Se@Si[O.sub.2] NPs in various metabolic disorders and inflammatory diseases. Conclusion: This study brought new insights into mitochondria-targeting bioactive NPs, with application potential in curing ALI or other human mitochondria-related disorders. Keywords: mitochondrial dysfunction, porous Se@Si[O.sub.2] nanoparticles, acute lung injury, anti-oxidative injury, anti-inflammation
ISSN:1178-2013
1178-2013
DOI:10.2147/IJN.S240301