The functions of a new WD-repeat domain containing protein naofen to modulate LPS-induced liver dysfunction

内毒素（LPS）引起肝细胞凋亡和肝功能障碍，如脓毒症所述。因此，在这项研究中，我们研究了一个新的含有蛋白naofen （WDR35）的WD-repeat结构域在lps诱导的肝功能障碍中的功能。LPS激活Kuppfer细胞并释放细胞因子，如tnf - α。然后增加肝细胞naofen mRNA和蛋白的表达。Naofen/WDR35抑制抗凋亡蛋白Bcl-2和Bcl-xL的表达，促进肝细胞凋亡。提示脑啡肽可能参与内毒素肝损伤，可作为内毒素肝损伤治疗的新靶点。

Endothxin (LPS) causes hepatocytic apoptosis and liver dysfunction, as described in cases of sepsis. In this study, we therefore investigated the functions of a new WD-repeat domain containing protein naofen (WDR35) in LPS-induced liver dysfunction. LPS activated Kuppfer cells and released cytokines, such as TNF-alpha. Which then increased mRNA and protein expression of naofen in hepatocytes. Naofen/WDR35 inhibited expressions of anti-apoptotic proteins Bcl-2 and Bcl-xL, and stimulated apoptosis of hepatocytes. These results suggested that naofen may be involved in endotoxin-induced liver injury, and as a new therapeutic targets for endotoxin-induced liver injury therapy.