Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide, and scientific studies consistently report that NAFLD development can be accelerated by oxidative stress. Oxidative stress can induce the progression of NAFLD to NASH by stimulating Kupffer cells, hepatic stellate cells, and hepatocytes. Therefore, studies are underway to identify the role of antioxidants in the treatment of NAFLD. In this review, we have summarized the origins of reactive oxygen species (ROS) in cells, the relationship between ROS and NAFLD, and have discussed the use of antioxidants as therapeutic agents for NAFLD.
Highlights
Nonalcoholic fatty liver disease (NAFLD) progresses from simple steatosis to steatohepatitis, fibrosis, cirrhosis, and to HCC due to insulin resistance, hepatic oxidative stress (OS), and lipotoxicity mediated by a longterm western diet [46]
Cells In associated Liver Disease (ALD) and NAFLD, intestinal endotoxin/LPS is the main stimulator of Kupffer cells (KCs) activation, In ALD and NAFLD, intestinal endotoxin/LPS is the main stimulator of KC activawhich results in the production of pro-inflammatory factors, chemokines and abundant reactive oxygen species (ROS)
These results suggest that the induction of OGT and glutamine: fructose-6-phosphate amidotransferase (GFAT) by the transcriptional regulation of X-box binding protein 1 (XBP1) (which is as an upstream activator of hexosamine biosynthetic pathway (HBP)) activates a positive regulatory loop in NASH pathogenesis
Summary
Nonalcoholic Fatty Liver Disease (NAFLD) is the most common chronic liver disease, and a large proportion of the population worldwide has it [1]. NAFLD is defined as an accumulation of fat (>5%) in the liver cells in the absence of excessive alcohol consumption or other causes of liver disease, including autoimmune disease, drug-induced conditions, or viral hepatitis [2]. Alcohol-associated Liver Disease (ALD) and NAFLD are the most common causes of chronic liver disease. They share a common spectrum of fatty liver/steatosis, steatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma, several differences exist [3]. Most of the free fatty acids (FFAs) stored as TGs result from increased lipolysis in peripheral tissues This increased lipolysis is a consequence of hyperinsulinemia and dietary fat that induce insulin resistance (IR), and increased lipogenesis. NASH is a pro-inflammatory state that leads to the activation of Kupffer cells (KCs) and astrocytes, which stimulate collagen deposition, leading to liver fibrosis [9,10]
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