论文部分内容阅读
非酒精性脂肪性肝病(NAFLD)已被认为是一种慢性低度炎性反应状态[1],炎性反应在其复杂的发病机制中至关重要,是疾病向终末期肝病进展的关键。锌指蛋白A20是由核因子-κB(NF-κB)激活诱导的炎性反应负性调节蛋白,它通过可逆的去泛素化以及泛素化功能下调活化的NF-κB信号通路,从而抑制炎性反应[2]。近年来研究发现,A20对肝脏再生及功能恢复具有积极作用,可抑制肝损伤、
Non-alcoholic fatty liver disease (NAFLD) has been considered a chronic, low-grade inflammatory response [1]. Inflammatory responses are crucial in their complex pathogenesis and are key to the progression of the disease to end-stage liver disease. Zinc Finger Protein A20 is a negative regulator of inflammatory response induced by activation of nuclear factor-kappa B (NF-κB), which inhibits the activation of NF-κB signaling through reversible deubiquitination and ubiquitination Inflammatory reaction [2]. In recent years, the study found that A20 has a positive effect on liver regeneration and functional recovery, can inhibit liver injury,