非酒精性脂肪肝的抗氧化机制

Title:Antioxidant Mechanisms in Nonalcoholic Fatty Liver Disease

Volume: 16 Issue: 12

Author(s): Wensheng Liu, Susan S Baker, Robert D Baker and Lixin Zhu

Affiliation:

关键词: 抗氧化，酒精代谢，脂肪酸氧化，脂质代谢，非酒精性脂肪肝，非酒精脂肪性肝炎，氧化应激，活性氧。

摘要: Nonalcoholic fatty liver disease (NAFLD) represents a broad spectrum of histological abnormalities with clinical presentations ranging from hepatic steatosis to nonalcoholic steatohepatitis (NASH). Some NAFLD patients may progress to cirrhosis and ultimately hepatocellular carcinoma (HCC). Hepatic steatosis, the hallmark of NAFLD, is defined by the accumulation of triglycerides (TGs) in more than 5% of the hepatocytes. NASH is characterized by inflammation along with variable degrees of fibrosis in addition to steatosis. NAFLD has been considered to be the hepatic manifestation of metabolic syndrome (MS), as it is frequently associated with MS conditions such as insulin resistance (IR) and obesity. Hepatic steatosis mainly results from disrupted homeostasis of lipid metabolism in the setting of IR. Although the mechanism underlying the progression from steatosis to NASH is still not fully elucidated, mounting evidence has suggested oxidative stress (OS) to be a key driving force. Elevated OS has been well documented in NAFLD patients. OS can cause direct damages to lipid, protein, and DNA molecules and trigger the inflammatory and fibrogenesis signaling pathways, which promotes the progression from steatosis to NASH. OS may also have various effects on antioxidant defense mechanisms. Overproduced reactive oxygen species (ROS) may directly deplete antioxidant molecules such as glutathione (GSH) and inhibit the activities of antioxidant enzymes such as superoxide dismutase (SOD). ROS may also induce the expression of antioxidant genes to counteract the OS effects. The aim of this review is to discuss oxidative stress and antioxidant mechanisms in NAFLD.

Cite this article as:

Wensheng Liu, Susan S Baker, Robert D Baker and Lixin Zhu , Antioxidant Mechanisms in Nonalcoholic Fatty Liver Disease, Current Drug Targets 2015; 16 (12) . https://dx.doi.org/10.2174/1389450116666150427155342