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Sodium Propionate Enhances Nrf2-Mediated Protective Defense Against Oxidative Stress and Inflammation in Lipopolysaccharide-Induced Neonatal Mice. | LitMetric

AI Article Synopsis

  • - The study explores how sodium propionate (SP), a short-chain fatty acid, can counteract bronchopulmonary dysplasia (BPD) caused by inflammation and oxidative stress, particularly looking at its effects on neonatal mice and pulmonary cells.
  • - SP treatment led to increased Nrf2 expression and decreased inflammation and oxidative stress in LPS-induced BPD models, enhancing cell viability and angiogenesis in lung cells.
  • - The protective effects of SP were shown to be dependent on the Nrf2 pathway, as inhibiting Nrf2 negated the benefits of SP, suggesting its crucial role in combating BPD-related changes.

Article Abstract

Background: Alveolar arrest and the impaired angiogenesis caused by chronic inflammation and oxidative stress are two main factors in bronchopulmonary dysplasia (BPD). Short-chain fatty acids (SCFAs), especially propionate, possess anti-oxidant and anti-inflammatory effects. The present study was designed to examine the roles of sodium propionate (SP) on lipopolysaccharide (LPS)-challenged BPD and its potential mechanisms.

Methods: WT, Nrf2 mice and pulmonary microvascular endothelial cells (HPMECs) were used in this study. LPS was performed to mimic BPD model both in vivo and vitro. Lung histopathology, inflammation and oxidative stress-related mRNA expressions in lungs involved in BPD pathogenesis were investigated. In addition, cell viability and angiogenesis were also tested.

Results: The increased nuclear factor erythroid 2-related factor (Nrf2) and decreased Kelch-like ECH-associated protein-1 (Keap-1) expressions were observed after SP treatment in the LPS-induced neonatal mouse model of BPD. In LPS-induced wild-type but not Nrf2 neonatal mice, SP reduced pulmonary inflammation and oxidative stress and exhibited obvious pathological alterations of the alveoli. Moreover, in LPS-evoked HPMECs, SP accelerated Nrf2 nuclear translocation presented and exhibited cytoprotective and pro-angiogenesis effects. In addition, SP diminished the LPS-induced inflammatory response by blocking the activation of nuclear factor-kappa B pathway. Moreover, pretreatment with ML385, an Nrf2 specific inhibitor, offsets the beneficial effects of SP on inflammation, oxidative stress and angiogenesis in LPS-evoked HPMECs.

Conclusion: SP protects against LPS-induced lung alveolar simplification and abnormal angiogenesis in neonatal mice and HPMECs in an Nrf2-dependent manner.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7957230PMC
http://dx.doi.org/10.2147/JIR.S303105DOI Listing

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