4.7 Article

Gold Nanoparticles Inhibit Steroid-Insensitive Asthma in Mice Preserving Histone Deacetylase 2 and NRF2 Pathways

期刊

ANTIOXIDANTS
卷 11, 期 9, 页码 -

出版社

MDPI
DOI: 10.3390/antiox11091659

关键词

gold nanoparticle; steroid-insensitive asthma; lung inflammation; NRF2; HDAC2; oxidative imbalance

资金

  1. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brasiilia, Brazil [315924/2020-9]
  2. Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ), Rio de Janeiro, Brazil [PENSA-RIO-E26/010.003028/2014, E-26/010.101054/2018]
  3. Instituto Nacional de Ciencia e Tecnologia-INOFAR, Rio de Janeiro and Brasilia, Brazil [465249/2014-0]
  4. FAPERJ [E-26/200.868/2018]
  5. Rede Rio de Inovacao em Nanosistemas para Saude (Nano-Saude/FAPERJ) [E-26/010.000983/2019]

向作者/读者索取更多资源

This study found that nebulized gold nanoparticles (AuNPs) can improve steroid-insensitive asthma by preserving HDAC2 and NRF2 levels, reducing oxidative stress and inflammation.
Background: Gold nanoparticles (AuNPs) can inhibit pivotal pathological changes in experimental asthma, but their effect on steroid-insensitive asthma is unclear. The current study assessed the effectiveness of nebulized AuNPs in a murine model of glucocorticoid (GC)-resistant asthma. Methods: A/J mice were sensitized and subjected to intranasal instillations of ovalbumin (OVA) once a week for nine weeks. Two weeks after starting allergen stimulations, mice were subjected to Budesonide or AuNP nebulization 1 h before stimuli. Analyses were carried out 24 h after the last provocation. Results: We found that mice challenged with OVA had airway hyperreactivity, eosinophil, and neutrophil infiltrates in the lung, concomitantly with peribronchiolar fibrosis, mucus production, and pro-inflammatory cytokine generation compared to sham-challenged mice. These changes were inhibited in mice treated with AuNPs, but not Budesonide. In the GC-resistant asthmatic mice, oxidative stress was established, marked by a reduction in nuclear factor erythroid 2-related factor 2 (NRF2) levels and catalase activity, accompanied by elevated values of thiobarbituric acid reactive substances (TBARS), phosphoinositide 3-kinases delta (PI3K delta) expression, as well as a reduction in the nuclear expression of histone deacetylase 2 (HDAC2) in the lung tissue, all of which sensitive to AuNPs but not Budesonide treatment. Conclusion: These findings suggest that AuNPs can improve GC-insensitive asthma by preserving HDAC2 and NRF2.

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