花生四烯酸氧化应激与非酒精性脂肪性肝病的研究进展

The study progress of arachidonic acid oxidative stress and non-alcoholic fatty liver disease

非酒精性脂肪性肝病(NAFLD)"二次打击学说"认为,氧化应激、脂质过氧化在肝细胞损伤过程中起重要作用。花生四烯酸(AA)作为重要的炎性脂质介质,通过环氧化酶(COX)、脂氧合酶(LOX)、细胞色素P450三大代谢途径来调控肝细胞线粒体内的氧化应激,导致大量脂酸的氧化及脂质过氧化物的形成,肝内胶原的沉积,加重肝细胞的损伤和肝星状细胞(HSC)激活,最终加快NAFLD进展。通过对AA介导的氧化应激在NAFLD发病机制中作用的进一步深入研究,有可能探索出有效治疗脂肪性肝病的新途径,为阻断NAFLD进展提供有力的理论依据。

NAFLD＇s ＂second-hit theory＂ demonstrated that oxidative stress and lipid peroxidation played an impor- tant role in the liver cell damage.Arachidonic acid （AA）,an important inflammatory lipid mediator,can regulate liver mitochondria oxidative stress by the cyclooxygenase （COX）,lipoxygenase （LOX） and eytochrome P450 metabolic pathways.AA could lead to fatty acid oxidation,lipid peroxide formation, liver collagen deposition and increased liver cell damage and hepatic stellate cells （HSC） activation.This ultimately accelerated the progress of NAFLD. It will provide a theoretical basis of blocking NAFLD progress.