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SPAUTIN-1 alleviates LPS-induced acute lung injury by inhibiting NF-κB pathway in neutrophils. | LitMetric

SPAUTIN-1 alleviates LPS-induced acute lung injury by inhibiting NF-κB pathway in neutrophils.

Int Immunopharmacol

Zhejiang Key Laboratory of Interventional Pulmonology, Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China. Electronic address:

Published: March 2024

AI Article Synopsis

  • - The study investigates the protective effects of SPAUTIN-1, a small molecule drug, on acute lung injury (ALI), focusing on its mechanisms in pulmonary inflammatory responses and oxidative stress.
  • - Using lipopolysaccharides (LPS) to induce inflammation and bleomycin for non-inflammation-mediated ALI, researchers found that SPAUTIN-1 significantly reduced lung injury and inflammatory responses linked to LPS, while having no effect on bleomycin-induced injury.
  • - Results showed that SPAUTIN-1 inhibits the NF-κB signaling pathway in leukocytes and mitigates oxidative stress in lung epithelial cells, suggesting its potential as a therapeutic candidate for treating ALI.

Article Abstract

Background: Acute lung injury (ALI) is an inflammatory condition characterized by acute damage to lung tissue. SPAUTIN-1, recognized as a small molecule drug targeting autophagy and USP10/13, has been reported for its potential to inhibit oxidative stress damage in various tissue injuries. However, the role and mechanism of SPAUTIN-1 in ALI remain unclear. This study aims to elucidate the protective effects of SPAUTIN-1 on ALI, with a particular focus on its role and mechanism in pulmonary inflammatory responses.

Methods: Lipopolysaccharides (LPS) were employed to induce inflammation-mediated ALI. Bleomycin was used to induce non-inflammation-mediated ALI. The mechanism of SPAUTIN-1 action was identified through RNA-Sequencing and subsequently validated in mouse primary cells. Tert-butyl hydroperoxide (TBHP) was utilized to create an in vitro model of lung epithelial cell oxidative stress with MLE-12 cells.

Results: SPAUTIN-1 significantly mitigated LPS-induced lung injury and inflammatory responses, attenuated necroptosis and apoptosis in lung epithelial cells, and inhibited autophagy in leukocytes and epithelial cells. However, SPAUTIN-1 exhibited no significant effect on bleomycin-induced lung injury. RNA-sequencing results demonstrated that SPAUTIN-1 significantly inhibited the NF-κB signaling pathway in leukocytes, a finding consistently confirmed by mouse primary cell assays. In vitro experiments further revealed that SPAUTIN-1 effectively mitigated oxidative stress injury in MLE-12 cells induced by TBHP.

Conclusion: SPAUTIN-1 alleviated LPS-induced inflammatory injury by inhibiting the NF-κB pathway in leukocytes and protected epithelial cells from oxidative damage, positioning it as a potential therapeutic candidate for ALI.

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Source
http://dx.doi.org/10.1016/j.intimp.2024.111741DOI Listing

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