The H3K4me3 pattern of mouse renal cortex tissues treated with dexmedetomidine against lipopolysaccharide-induced sepsis
Dexmedetomidine (DEX) was served to controlling the over-reactive inflammatory effects to protect from the sepsis-induced organ failure via modulating histone methylation. However, the genome-wide changes of histone methylations upon DEX for sepsis treatment were poorly explored. (AKI) mouse model was induced by lipopolysaccharide (LPS), and added DEX (AKI+D) and KDM5A-IN-1 (KDM5A inhibitor) (AKI+K) respectively. ChIP-seq to investigate the H3K4me3 pattern in renal cortex tissues. Each group has two replications.