ArticleFrontiers in pharmacology2025
Liver X receptor agonist T0901317 alleviates sepsis-induced acute lung injury by enhancing macrophage autophagy.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: This study was aimed at identifying the effects of liver X receptor alpha (LXRα) on sepsis-induced acute lung injury (ALI) and clarifying its novel regulatory mechanisms using bioinformatics and experimental methods. Methods: Bioinformatics analysis of the differentially expressed genes and functional annotations were performed. Lipopolysaccharide (LPS) was administered intraperitoneally for sepsis-induced ALI in a mouse model; then, the LXR agonist T0901317 (T0) was administered to the mice along with RAW264.7 macrophages for LXRα activation. We then performed hematoxylin and eosin staining, estimated the total protein in the bronchoalveolar lavage fluid, and detected the expressions of TNFα and IL6 by reverse transcription polymerase chain reaction to evaluate the inflammatory injury in the lung tissues. Autophagy was detected via immunohistochemistry, transmission electron microscopy, and Western blotting. RNA sequencing was then used to analyze the autophagy-related genes regulated by LXRα, and the cells were transfected with S100A8-siRNA to determine whether LXRα regulated inflammatory damage by regulating the autophagy-related gene S100A8. The clinical correlation between LXRα and S100A8 was determined through analysis of human transcriptome data. Results: The bioinformatics analyses revealed that LXRα (NR1H3) was downregulated in sepsis-induced ALI models and that LXRα might regulate autophagy. The animal- and cell-based experiments further verified these findings. The LXR agonist T0 was found to alleviate lung damage and reduce the expressions of inflammatory factors in the lung tissues and cells. After inhibiting autophagy with 3-methyladenine, the protective effects of T0 on inflammatory damage were shown to be inhibited. Subsequently, RNA sequencing of the macrophages was performed, and four genes ( Conclusion: The findings of this study suggest that T0 attenuates sepsis-induced pulmonary injury by promoting macrophage autophagy via suppression of S100A8 expression.
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