Effects of binge ethanol on lipid homeostasis and oxidative stress in a rat model of nonalcoholic fatty liver disease

2014 ◽  
Author(s):  
Elena Grasselli ◽  
Adriana Voci ◽  
Ilaria Demori ◽  
Rita De Matteis ◽  
Andrea D. Compalati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Rat Model ◽  
Fatty Liver Disease ◽  
Lipid Homeostasis ◽  
Nonalcoholic Fatty Liver ◽  
Binge Ethanol ◽  
And Oxidative Stress

scholarly journals A High-Fat, High-Fructose Diet Induces Antioxidant Imbalance and Increases the Risk and Progression of Nonalcoholic Fatty Liver Disease in Mice

Scientifica ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Kanokwan Jarukamjorn ◽  
Nattharat Jearapong ◽  
Charinya Pimson ◽  
Waranya Chatuphonprasert
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
High Fructose Diet ◽  
High Fructose ◽  
And Oxidative Stress

Excessive fat liver is an important manifestation of nonalcoholic fatty liver disease (NAFLD), associated with obesity, insulin resistance, and oxidative stress. In the present study, the effects of a high-fat, high-fructose diet (HFFD) on mRNA levels and activities of the antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), were determined in mouse livers and brains. The histomorphology of the livers was examined and the state of nonenzymatic reducing system was evaluated by measuring the glutathione system and the lipid peroxidation. Histopathology of the liver showed that fat accumulation and inflammation depended on the period of the HFFD-consumption. The levels of mRNA and enzymatic activities of SOD, CAT, and GPx were raised, followed by the increases in malondialdehyde levels in livers and brains of the HFFD mice. The oxidized GSSG content was increased while the total GSH and the reduced GSH were decreased, resulting in the increase in the GSH/GSSG ratio in both livers and brains of the HFFD mice. These observations suggested that liver damage and oxidative stress in the significant organs were generated by continuous HFFD-consumption. Imbalance of antioxidant condition induced by long-term HFFD-consumption might increase the risk and progression of NAFLD.

scholarly journals P- Hydroxybenzyl Alcohol Alleviates Oxidative Stress in a Nonalcoholic Fatty Liver Disease Larval Zebrafish Model and a BRL-3A Hepatocyte Via the Nrf2 Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Jing An ◽  
Lijun Cheng ◽  
Liping Yang ◽  
Nali Song ◽  
Ju Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Larval Zebrafish ◽  
And Oxidative Stress ◽  
Lipid Regulation

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and it has gradually become the main disease burden in the world. However, the pathogenesis of NAFLD is complex, involving such things as dyslipidemia, oxidative stress, inflammation, etc. This brings to the table a significant challenge for drug development, and there is still no drug approved by the FDA on the market to treat the disease. GAS and HBA are active ingredients of the orchidaceae plant gastrodia elata and have exhibit effects in ameliorating nervous system diseases caused by oxidative stress. HBA is a metabolite of GAS that could perform lipid regulation and improve oxidative stress on HCD-induced NAFLD larval zebrafish, as reported by previous studies; we therefore explored the role of HBA in lipid regulation and oxidative stress on HCD-induced NAFLD larval zebrafish in vivo and FFA-induced BRL-3A hepatocyte in vitro. The gene expression of lipogenesis, inflammation, and oxidative stress were measured to investigate the underlying mechanism of HBA, and the potential protein target of HBA was explored by immunofluorescence. Altogether, our data highlight the role of HBA in improving NAFLD by use of its lipid-lowering and anti-oxidative properties via the Nrf2/HO-1 signaling pathway, providing a potential therapeutic compound for NAFLD treatment.

Diet-induced dyslipidemia leads to nonalcoholic fatty liver disease and oxidative stress in guinea pigs

2016 ◽  
Vol 168 ◽  
pp. 146-160 ◽  
Author(s):  
Pernille Tveden-Nyborg ◽  
Malene M. Birck ◽  
David H. Ipsen ◽  
Tina Thiessen ◽  
Linda de Bie Feldmann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Guinea Pigs ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
And Oxidative Stress

scholarly journals Capybara Oil Improves Hepatic Mitochondrial Dysfunction, Steatosis, and Inflammation in a Murine Model of Nonalcoholic Fatty Liver Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Polyana C. Marinho ◽  
Aline B. Vieira ◽  
Priscila G. Pereira ◽  
Kíssila Rabelo ◽  
Bianca T. Ciambarella ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Mitochondrial Dysfunction ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Positive Effects ◽  
And Oxidative Stress

Nonalcoholic fatty liver disease (NAFLD) is recognized as the most common cause of liver dysfunction worldwide and is commonly associated with obesity. Evidences suggest that NAFLD might be a mitochondrial disease, which contributes to the hepatic steatosis, oxidative stress, cytokine release, and cell death. Capybara oil (CO) is a rich source of polyunsaturated fatty acids (PUFA), which is known to improve inflammation and oxidative stress. In order to determine the effects of CO on NAFLD, C57Bl/6 mice were divided into 3 groups and fed a high-fat diet (HFD) (NAFLD group and NAFLD + CO group) or a control diet (CG group) during 16 weeks. The CO (1.5 g/kg/daily) was administered by gavage during the last 4 weeks of the diet protocol. We evaluated plasma liver enzymes, hepatic steatosis, and cytokine expression in liver as well as hepatocyte ultrastructural morphology and mitochondrial function. CO treatment suppressed hepatic steatosis, attenuated inflammatory response, and decreased plasma alanine aminotransferase (ALT) in mice with NAFLD. CO was also capable of restoring mitochondrial ultrastructure and function as well as balance superoxide dismutase and catalase levels. Our findings indicate that CO treatment has positive effects on NAFLD improving mitochondrial dysfunction, steatosis, acute inflammation, and oxidative stress.

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