姜黄素缓解乙醇诱导的肝细胞脂肪变性的分子机制研究
摘要：目的对近年来关于减少肝细胞脂质变性在酒精肝防治中的作用进行整理分析。方法查阅近年来的国内外文献，进行全面综合、整理和归纳。结果综述了肝细胞脂质变性在酒精肝发生发展中的重要意义，全面阐述肝细胞表面的脂滴并重点阐述可能存在的调控因子。结论减少肝细胞脂质变性在酒精肝防治中具有重要作用，但其作用机制亟待进一步研究。
关键词：酒精肝；姜黄素；脂质积聚；Nrf2; FXR
Curcumin Attenuates Ethanol-induced Hepatic Steatosis through Modulating Nrf2/FXR Signaling in Hepatocytes
ABSTRACT: OBJECTIVE We have analyzed recent studies on the induction of lipocyte phenotype in activated hepatic stellate cell. METHODS We have read domestic and international documents in recent years. Then we concluded a comprehensive integrated about them. RESULTS This paper reviews the importance of the potential strategy for the treatment of liver fibrosis by inducing the lipocyte phenotype in activated hepatic stellate cell, which focuses on the lipid droplets and the potential regulators. CONCLUSION Induction of lipocyte phenotype in activated hepatic stellate cell is very important in treating liver fibrosis. But for its complex mechanism of action, we need further research.
KEY WORDS:alcoholic liver disease; curcumin; lipid accumulation; Nrf2; FXR
酒精肝是继发于各种慢性肝损伤之后组织修复过程中的代偿反应，涉及多种细胞因子、炎性趋化因子、生长因子、打破肝脏内的稳态平衡[1]。肝星状细胞（hepatic stellate cell，HSC）是酒精肝细胞外基质（excellular matrix，ECM）最主要的细胞来源。现已经公认HSC活化是酒精肝发生发展的核心环节。针对HSC为靶标干预成为抗酒精肝的重要措施及研究热点。目前研究表明，诱导活化型HSC静息态脂肪表型可以减少ECM分泌，促进酒精肝的恢复。目前，关于从抑制HSC增殖，促进ECM降解的综述已经有较多，而HSC静息态脂肪细胞表型的消失是HSC所有表型改变中最具独特性的，并且对于静息态脂肪细胞表型在酒精肝中的研究起步较晚，因此，本文将深入阐述HSC脂滴的生物合成和生长及其对抗酒精肝的潜在重要性，为进一步研究诱导HSC静息态脂肪细胞表型打下基础。
1. 静息态肝星状细胞脂肪细胞表型的分化
