The present study aimed to evaluate the effects of ethanol extract (BTEE) on lipopolysaccharide (LPS)-induced inflammation in RAW264 cells. BTEE significantly attenuated LPS-induced nitric oxide production and inflammatory cytokines release, including , , and . On the other hand, several anti-inflammatory mediators, such as and , were increased in BTEE-treated cells. Further, we performed an untargeted whole-genome microarray analysis to explore the anti-inflammatory molecular mechanism of BTEE. Enrichment analysis showed BTEE significantly downregulated 'response to stimulus', 'locomotion', and 'immune system response' and upregulated 'cell cycle' gene ontologies in both 6- and 17-h post-LPS stimulation conditions. Pathway analysis revealed BTEE could downregulate the expressions of chemokines of the CC and CXC subfamily, and cytokines of the TNF family, TGFβ family, IL1-like, and class I helical. PPI analysis showed AXL receptor tyrosine kinase (), a receptor tyrosine kinase from the TAM family, and its upstream transcription factors were downregulated in both conditions. Node neighborhood analysis showed several coexpressed genes were also downregulated. Further, kinase enrichment and chemical perturbation analyses supported inhibition in BTEE-treated conditions. Altogether, these findings suggest anti-inflammatory effects of BTEE that are mediated via the suppression of pro-inflammatory cytokines and predict its potential as an inhibitor.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10095501PMC
http://dx.doi.org/10.3390/ijms24076666DOI Listing

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