1477 Sodium butyrate promotes diabetic tissue repair through resetting the epigenetic machinery of macrophages

Wound healing disorders including diabetic ulcers, chronic venous leg ulcers and pressure are still remains uncured pose a stern challenge to health care system. Accumulation of dysfunctional macrophages over time have been identified as major underlying cause for wounds, however molecular events regulating these unclear. In present study, we found that histone H3K27 acetylation, an epigenetic mark macrophage transcriptome, suppressed under inflammatory microenvironment. Employing series ofin vitro in vivoexperiments microenvironment markedly the acetylation by activating deacetylase-dependent pathways. addition, observed shift transcription control from STAT1 JUN palmitate-exposed stimulated macrophages. Of note, deacetylase inhibitor sodium butyrate enhanced skin wounds via restoring acetylation-dependent pathways wound associated-macrophages reinstalled signaling. Furthermore, inhibition preserved morphological features well improved phagocytic migratory activity Our study reveals novel pathogenic mechanism controlling perturbed macrophages, which can be therapeutically exploited cure dominated unrestrained macrophage.