Transcriptomic profiling of differentially expressed mRNA in liver tissue of Dgaln/LPS induced liver injury mice [mRNA_Dgaln]

Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide(Dgaln/lps), APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates Dgaln/lps-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against Dgaln/lps-induced hepatocyte injury. Overall design: RNA-seq was conducted on total RNA isolated from livers of AILI mice treated with D-GalN 500mg/kg, LPS 5µg/kg or dmPGE2 300µg/kg for 6 h; n = 3 per group except dmPGE2+Dgaln/LPS group. The number of samples in dmPGE2+Dgaln/LPS group is 4.

急性肝衰竭（Acute liver failure）是突发性肝损伤引发的严重临床综合征，可由多种因素诱发。既往研究表明，前列腺素E2（PGE2）可显著缓解由半乳糖胺/脂多糖（D-galactosamine/lipopolysaccharide，DGaln/LPS）、对乙酰氨基酚（APAP）及四氯化碳（carbon tetrachloride）诱导的急性肝衰竭。然而，PGE2缓解DGaln/LPS诱导的急性肝衰竭的具体分子机制仍未阐明。本研究旨在探究PGE2对抗DGaln/LPS诱导的肝细胞损伤的保护作用机制。
总体实验设计：对经D-半乳糖胺（D-GalN）500mg/kg、脂多糖（LPS）5μg/kg或二甲基前列腺素E2（dmPGE2）300μg/kg处理6小时的急性肝损伤（AILI）小鼠肝脏分离的总RNA进行RNA测序（RNA-seq）；除dmPGE2+Dgaln/LPS组外，每组样本量均为3，该组样本量为4。