非酒精的脂肪肝疾病(NAFLD ) 是新陈代谢的症候群的肝的表明并且包括肝的脂肪变性, steatohepatitis,和纤维变性的一个系列。Interleukin-17 (IL-17 ) 被报导了在一些肝疾病的煽动性的前进起一个关键作用。现在的学习被设计在 C57BL/6 老鼠在高胖的导致食谱的 NAFLD 上调查 IL-17 的角色。有 anti-IL-17mAb 的 IL-17 封锁 signicantly 改进了肝功能,稀释了肝的类脂化合物累积,压制了 Kuffer 房间激活,并且减少支持 inflammatory cytokines 铺平激活,它与表明串联的 NF-B 的抑制被联系。我们的数据建议 IL-17 与在 NAFLD 老鼠模型的疾病前进有关,堵住 IL-17 可以是为有 NAFLD 的病人的一条有希望的新奇治疗学的途径。
Non-alcoholic fatty liver disease (NAFLD) is hepatic manifestation of a metabolic syndrome and includes a spec- trum of hepatic steatosis, steatohepatitis, and fibrosis. Interleukin-17 (IL-17) has been reported to play a critical role in inflammatory progression of some liver diseases. The present study was designed to investigate the role of IL-17 on high fat diet-induced NAFLD in C57BL/6 mice. IL-17 blockade with anti-IL-17mAb significantly improved liver function, attenuated hepatic lipid accumulation, suppressed Kuffer cells activation, and decreased pro- inflammatory cytokines levels, which were associated with inhibition of NF-κB signafing cascades activation. Our data suggested that IL-17 was related to disease progression in NAFLD mouse model and blocking IL-17 may be a promis- ing novel therapeutic approach for patients with NAFLD.