Transcriptomic profiling of mouse colorectal organoids following NAP treatment.

In this study, we investigated the impact of BPF exposure on the intestinal barrier and cardiovascular system. Based on prior untargeted metabolomic analysis, we revealed that BPF can be converted into N-acetylputrescine (NAP) through a microbiota-associated metabolic process.

Further experiments demonstrated that BPF exposure stimulated intestinal epithelial cells to secrete spermidine/spermine N1-acetyltransferase 1 (Sat1), an enzyme involved in this conversion. To explore the molecular mechanisms underlying NAP-induced effects, we performed RNA sequencing on mouse colorectal organoids treated with NAP. Transcriptomic analysis was conducted to identify gene expression changes and signaling pathways associated with NAP exposure.