PGC-1β拮抗LPS诱导的肝脏Hepcidin表达升高及铁过度堆积

PGC-1β Antagonizes LPS-Induced Hepcidin Expression and Iron Accumulation in Liver

探讨PGC-1β在调节肝脏Hepcidin表达及铁代谢稳态中的作用.在脂多糖(Lipopolysaccharides,LPS)处理的小鼠肝脏和原代肝细胞中,通过RT-q PCR和Western Blot实验检测PGC-1β及Hepcidin的表达.使用腺病毒介导的过表达和干扰手段,研究PGC-1β对本底及LPS刺激下Hepcidin表达的影响.最后,通过普鲁士蓝染色法探究PGC-1β对LPS刺激后肝脏铁离子堆积的影响.结果表明:(1)LPS在体内和体外水平,均可显著抑制PGC-1β的表达,而增加Hepcidin的表达;(2)过表达PGC-1β能抑制LPS诱导的Hepcidin表达及胞内铁堆积.综上,PGC-1β可以拮抗LPS诱导的Hepcidin表达升高及铁的过度堆积.

This study is aimed to investigate the effect of PGC-1β on LPS-induced Hepcidin expression and iron accumulation in liver. RT-qPCR and Western Blot analyses were used to detect the expression levels of PGC-1β and Hepcidin in mouse liver and primary hepatocytes treated with LPS. Gain- and loss-of-function studies were performed to assess the role of PGC-1β in the regulation of Hepcidin expression under basal and LPS-stimulated conditions. Finally, Perls ＇ Prussian blue staining was administrated to detect the effects of PGC-1β on LPS-induced hepatic iron deposition. Results showed that, （1）LPS caused a significant reduction in PGC-1β expression, whereas increased Hepcidin expression both in vivo and in vitro; （2）Over-expression of PGC-1β inhibited LPS-indueed Hepeidin expression and intracellular iron accumulation in liver. PGC-1β antagonizes LPS-induced Hepcidin expression and iron accumulation in liver.