TLR4受体的主要功能是参与先天免疫反应，但它还参与诸如炎症反应等其它一些重要的生理病理过程：如我们刚完成的国家自然科学基金项目（No.81272640）首次证实TLR4是参与肿瘤相关的新生血管形成的关键性分子之一；业已证实TLR4/NF-кB信号通路是导致内毒素诱发的肝脏损伤的关键。研究表明β-arrestin 2可以负性调控 TLR4/NF-кB通路；我们的研究首次表明内毒素激活TLR4可显著上调β-arrestin 2，这可能是控制过度炎症反应的一种反馈性抑制机制；据此我们合理假设β-arrestin 2可以保护、预防内毒素诱发的肝脏损伤。本研究拟对β-arrestin 2基因敲除的枯否细胞或过表达的巨噬细胞及TLR4功能失活的枯否细胞、β-arrestin 2基因敲除的小鼠及内毒素诱发的肝脏损伤患者三种研究对象，进行系列实验验证我们的假说，试图为防治内毒素诱发的肝损伤提供新靶点。

TLR4 receptor plays an important role in not only the innate immunity, but also a lot of other physio-pathological processes, such as endotoxin induced liver injury and tumor related angiogenesis which was proved by us with the support of National Natural Science Foundation of China (81272640). It has been shown that β-arrestin 2 can negatively regulate the TLR4/NF-кB pathway. Our study has shown that TLR4 activation by endotoxin up-relate the protein level of β-arrestin 2, this may be a negative feedback to control excessive activation of TLR4/NF-кB. Taken together, we hypothesized that β-arrestin 2 can prevent and protect endotoxin induced liver injury. A series of study will be performed on the Kupffer cells isolated from β-arrestin 2 knockout mice and mice with loss of TLR4 function, β-arresitn 2 over-expression RAW 264.7 cells, β-arrestin 2 knockout mice and patients with endotoxin induced liver injury to prove our hypothesis. β-arresitn 2 may be a new target for the prevention and treatment of endotoxin induced liver injury.