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Sodium propionate ameliorates lipopolysaccharide-induced acute respiratory distress syndrome in rats via the PI3K/AKT/mTOR signaling pathway. | LitMetric

AI Article Synopsis

  • - The study examines how sodium propionate (SP), a substance produced during the fermentation of dietary fiber, impacts acute respiratory distress syndrome (ARDS) in rats induced by lipopolysaccharide (LPS), focusing on lung function and inflammatory responses.
  • - Results showed that SP helped improve low oxygen levels and reduced lung and intestinal tissue damage by lowering pro-inflammatory markers like TNF-α and IL-6 while increasing the anti-inflammatory factor IL-10.
  • - SP also affected key cellular pathways by inhibiting the PI3K/AKT/mTOR signaling pathway and promoting autophagy, suggesting potential therapeutic benefits for ARDS related to inflammation and tissue repair.

Article Abstract

Acute respiratory distress syndrome (ARDS) is a severe lung disease characterized by significant hypoxemia, which impairs the oxygen supply necessary for optimal lung function. This study aimed to investigate the effects of sodium propionate (SP), the primary end product of intestinal flora fermentation of dietary fiber, on lipopolysaccharide (LPS)-induced ARDS in rats. The rats were treated with SP, after which the lung wet/dry ratio, arterial partial oxygen pressure (PaO), levels of pro- and anti-inflammatory cytokines, tight junction proteins ZO-1 and Occludin, as well as LC3 and phosphorylated PI3K (p-PI3K)/p-AKT/p-mTOR protein levels, were measured. Additionally, histopathological analysis was conducted. The results indicated that SP effectively alleviated arterial hypoxemia in rats and mitigated the pathological damage to both intestinal and lung tissues caused by LPS. Notably, SP significantly reduced the levels of inflammatory factors TNF-α and IL-6 in the blood and bronchoalveolar lavage fluid (BALF) of ARDS rats, while increasing the concentration of the anti-inflammatory factor IL-10. Furthermore, SP inhibited the activation of the PI3K/AKT/mTOR signaling pathway and enhanced the LC3II/LC3I ratio in lung tissue. Therefore, SP may improve LPS-induced ARDS in rats by inhibiting the activation of the PI3K/AKT/mTOR signaling pathway, promoting autophagy, decreasing the production and release of inflammatory markers, and reducing alveolar epithelial damage.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11525366PMC
http://dx.doi.org/10.1007/s13205-024-04130-3DOI Listing

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