scholarly journals A double-edged sword: The Kelch-like ECH-associated protein 1-nuclear factor erythroid-derived 2-related factor 2-antioxidant response element pathway targeted pharmacological modulation in nonalcoholic fatty liver disease

2021 ◽  
Vol 60 ◽  
pp. 281-290
Author(s):  
Yong-Lun Wang ◽  
Jiao Wu ◽  
Rui-Xi Li ◽  
Yu-Ting Sun ◽  
Yi-Jia Ma ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Antioxidant Response ◽  
Related Factor ◽  
Nuclear Factor ◽  
Antioxidant Response Element ◽  
Nonalcoholic Fatty Liver ◽  
Pharmacological Modulation

scholarly journals Zonarol Protected Liver from Methionine- and Choline-Deficient Diet—Induced Nonalcoholic Fatty Liver Disease in a Mouse Model

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3455
Author(s):  
Jia Han ◽  
Xin Guo ◽  
Tomoyuki Koyama ◽  
Daichi Kawai ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Inflammatory Responses ◽  
Oral Treatment ◽  
Control Group ◽  
Related Factor ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases with no approved treatment. Zonarol, an extract from brown algae, has been proven to have anti-inflammatory and antioxidant effects. In this study, we investigated the role of zonarol in the progression of methionine- and choline-deficiency (MCD) diet-induced NAFLD in mice. After oral treatment with zonarol, a lighter body weight was observed in zonarol group (ZG) mice in comparison to control group (CG) mice. The NAFLD scores of ZG mice were lower than those of CG mice. Hepatic and serum lipid levels were also lower in ZG mice with the reduced expression of lipid metabolism-related factors. Furthermore, ZG mice showed less lipid deposition, less inflammatory cell infiltration and lower inflammatory cytokine levels in comparison to CG mice. Moreover, the numbers of 8-hydroxy-20-deoxyguanosine (8-OHdG)-positive hepatocytes and levels of hepatic and serum thiobarbituric acid reactive substances (TBARS) were significantly lower in comparison to CG mice. The expression levels of nuclear factor erythroid 2 related factor 2 (Nrf2), as well as its upstream and downstream molecules, changed in ZG mice. Zonarol could prevent the progression of NAFLD by decreasing inflammatory responses, oxidative stress and improving lipid metabolism. Meanwhile the Nrf2 pathway may play an important role in these effects

scholarly journals The Dual Role of Nrf2 in Nonalcoholic Fatty Liver Disease: Regulation of Antioxidant Defenses and Hepatic Lipid Metabolism

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Sílvia S. Chambel ◽  
Andreia Santos-Gonçalves ◽  
Tiago L. Duarte
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Negative Regulator ◽  
Antioxidant Defenses ◽  
Related Factor ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is a progressive liver disease with ever-growing incidence in the industrialized world. It starts with the simple accumulation of lipids in the hepatocyte and can progress to the more severe nonalcoholic steatohepatitis (NASH), which is associated with inflammation, fibrosis, and cirrhosis. There is increasing awareness that reactive oxygen species and electrophiles are implicated in the pathogenesis of NASH. Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a positive regulator of the expression of a battery of genes involved in the protection against oxidative/electrophilic stress. In rodents, Nrf2 is also known to participate in hepatic fatty acid metabolism, as a negative regulator of genes that promote hepatosteatosis. We review relevant evidence in the literature that these two mechanisms may contribute to the protective role of Nrf2 in the development of hepatic steatosis and in the progression to steatohepatitis, particularly in young animals. We propose that age may be a key to explain contradictory findings in the literature. In summary, Nrf2 mediates the crosstalk between lipid metabolism and antioxidant defense mechanisms in experimental models of NAFLD, and the nutritional or pharmacological induction of Nrf2 represents a promising potential new strategy for its prevention and treatment.

scholarly journals Diversity in Antioxidant Response Enzymes in Progressive Stages of Human Nonalcoholic Fatty Liver Disease

2010 ◽  
Vol 38 (12) ◽  
pp. 2293-2301 ◽  
Author(s):  
Rhiannon N. Hardwick ◽  
Craig D. Fisher ◽  
Mark J. Canet ◽  
April D. Lake ◽  
Nathan J. Cherrington
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Antioxidant Response ◽  
Nonalcoholic Fatty Liver

scholarly journals Chemical Activators of the Nrf2 Signaling Pathway in Nonalcoholic Fatty Liver Disease

2021 ◽  
Vol 16 (1) ◽  
pp. 1934578X2098709
Author(s):  
Yinghua He ◽  
Jianping Jiang ◽  
Beihui He ◽  
Zheng Shi
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Signaling Pathway ◽  
Fatty Liver Disease ◽  
Research Progress ◽  
Related Factor ◽  
Nonalcoholic Fatty Liver ◽  
Cell Defense ◽  
Nrf2 Signaling Pathway

Nonalcoholic fatty liver disease (NAFLD) is paralleling the insulin resistance and obesity epidemic and is regarded as liver metabolic syndrome, and its prevalence rate is increasing rapidly. The best explanation for the occurrence and development of NAFLD is the “multiple hit” hypothesis instead of the “two-hit” hypothesis. At present, NAFLD therapies are limited. The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway is a key pathway in oxidative stress. Its downstream proteins/enzymes are regulated. Metabolic enzymes and antioxidant proteins/enzymes play a vital role in cell defense protection and have attracted attention in the field of antioxidant research in recent years. This paper summarizes the regulatory mechanism of the Nrf2 signaling pathway and the research progress of Nrf2 activators in NAFLD to provide guidance for NAFLD therapy in the future.

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