scholarly journals Silibinin ameliorates hepatic lipid accumulation and oxidative stress in mice with non-alcoholic steatohepatitis by regulating CFLAR-JNK pathway

2019 ◽  
Vol 9 (4) ◽  
pp. 745-757 ◽  
Author(s):  
Yayun Liu ◽  
Wei Xu ◽  
Ting Zhai ◽  
Jiaojiao You ◽  
Yong Chen
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
Jnk Pathway ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Alcoholic Steatohepatitis ◽  
And Oxidative Stress

scholarly journals Optimized Rapeseed Oils Rich in Endogenous Micronutrients Protect High Fat Diet Fed Rats from Hepatic Lipid Accumulation and Oxidative Stress

Nutrients ◽  
2015 ◽  
Vol 7 (10) ◽  
pp. 8491-8502 ◽  
Author(s):  
Jiqu Xu ◽  
Xiaoli Liu ◽  
Hui Gao ◽  
Chang Chen ◽  
Qianchun Deng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
And Oxidative Stress

scholarly journals N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1283
Author(s):  
Phiwayinkosi V. Dludla ◽  
Bongani B. Nkambule ◽  
Sithandiwe E. Mazibuko-Mbeje ◽  
Tawanda M. Nyambuya ◽  
Fabio Marcheggiani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
Randomized Clinical Trials ◽  
Therapeutic Potential ◽  
Therapeutic Effects ◽  
Metabolic Complications ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Acetyl Cysteine

Impaired adipose tissue function and insulin resistance remain instrumental in promoting hepatic lipid accumulation in conditions of metabolic syndrome. In fact, enhanced lipid accumulation together with oxidative stress and an abnormal inflammatory response underpin the development and severity of non-alcoholic fatty liver disease (NAFLD). There are currently no specific protective drugs against NAFLD, and effective interventions involving regular exercise and healthy diets have proved difficult to achieve and maintain. Alternatively, due to its antioxidant and anti-inflammatory properties, there has been growing interest in understanding the therapeutic effects of N-acetyl cysteine (NAC) against metabolic complications, including NAFLD. Here, reviewed evidence suggests that NAC blocks hepatic lipid accumulation in preclinical models of NAFLD. This is in part through the effective regulation of a fatty acid scavenger molecule (CD36) and transcriptional factors such as sterol regulatory element-binding protein (SREBP)-1c/-2 and peroxisome proliferator-activated receptor gamma (PPARγ). Importantly, NAC appears effective in improving liver function by reducing pro-inflammatory markers such as interleukin (IL)-6 IL-1β, tumour necrosis factor alpha (TNF-α) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). This was primarily through the attenuation of lipid peroxidation and enhancements in intracellular response antioxidants, particularly glutathione. Very few clinical studies support the beneficial effects of NAC against NAFLD-related complications, thus well-organized randomized clinical trials are still necessary to confirm its therapeutic potential.

scholarly journals Isoquercetin Improves Hepatic Lipid Accumulation by Activating AMPK Pathway and Suppressing TGF-β Signaling on an HFD-Induced Nonalcoholic Fatty Liver Disease Rat Model

2018 ◽  
Vol 19 (12) ◽  
pp. 4126 ◽  
Author(s):  
Guohong Qin ◽  
Ji Ma ◽  
Qiongshan Huang ◽  
Hongli Yin ◽  
Jichun Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Kupffer Cells ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid Accumulation ◽  
Ampk Pathway ◽  
And Oxidative Stress

Isoquercetin (IQ), a glucoside derivative of quercetin, has been reported to have beneficial effects in nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the potential improvement of IQ in liver lipid accumulation, inflammation, oxidative condition, and activation in Kupffer cells (KCs) on a high-fat diet (HFD) induced NAFLD models. Male Sprague-Dawley (SD) rats were induced by HFD, lipopolysaccharides/free fatty acids (LPS/FFA) induced co-culture cells model between primary hepatocytes and Kupffer cells was used to test the effects and the underlying mechanism of IQ. Molecular docking was performed to predict the potential target of IQ. Significant effects of IQ were found on reduced lipid accumulation, inflammation, and oxidative stress. In addition, AMP-activated protein kinase (AMPK) pathway was activated by IQ, and is plays an important role in lipid regulation. Meanwhile, IQ reversed the increase of activated KCs which caused by lipid overload, and also suppression of Transforming growth factor beta (TGF-β) signaling by TGF-β Recptor-1 and SMAD2/3 signaling. Finally, TGF-βR1 and TGF-βR2 were both found may involve in the mechanism of IQ. IQ can improve hepatic lipid accumulation and decrease inflammation and oxidative stress by its activating AMPK pathway and suppressing TGF-β signaling to alleviate NAFLD.

scholarly journals Fish oil prevents excessive hepatic lipid accumulation without inducing oxidative stress

2013 ◽  
Vol 88 (5) ◽  
pp. 365-371 ◽  
Author(s):  
Satoshi Hirako ◽  
Hyoun Ju Kim ◽  
Yuzuru Iizuka ◽  
Maki Nakasatomi ◽  
Akiyo Matsumoto
Keyword(s):  
Oxidative Stress ◽  
Fish Oil ◽  
Lipid Accumulation ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

scholarly journals Electromagnetic Fields Ameliorate Hepatic Lipid Accumulation and Oxidative Stress by Activating the CaMKKβ/AMPK/SREBP-1c and Nrf2 Pathways in High-Fat Diet-Fed Mice

2021 ◽  
Author(s):  
Mingming Zhai ◽  
Jinxiu Cui ◽  
Chenxu Zhang ◽  
Juan Liu ◽  
Yuanzhe Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Protein Expression ◽  
Electromagnetic Fields ◽  
High Fat Diet ◽  
Lipid Deposition ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
And Oxidative Stress

Abstract Background: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, and is related to disturbed lipid metabolism and redox homeostasis. However, a definitive drug treatment has not been approved for this disease. Studies have found that electromagnetic fields (EMFs) can ameliorate hepatic steatosis and oxidative stress. Nevertheless, the mechanism remains unclear.Methods: NAFLD models were established by feeding mice a high-fat diet. Simultaneously, EMF exposure is performed. The effects of the EMF on hepatic lipid deposition and oxidative stress were investigated. Additionally, the AMPK and Nrf2 pathways were analysed to confirm whether they were activated by the EMF.Results: Administration of the EMF decreased the body weight, liver weight and serum triglyceride (TG) levels and restrained the excessive hepatic lipid accumulation caused by feeding the HFD. This EMF function is achieved by boosting CaMKKβ protein expression, activating AMPK phosphorylation and suppressing mature SREBP-1c protein expression. Meanwhile, the activity of GSH-Px was enhanced following an increase in nuclear Nrf2 protein expression by EMF. However, no change was observed in the activities of SOD and CAT. Consequently, EMF reduced hepatic reactive oxygen species (ROS) and MDA levels, which means that EMF relieved liver damage by oxidative stress in HFD-fed mice.Conclusions: EMF can activate the CaMKKβ/AMPK/SREBP-1c and Nrf2 pathways to control hepatic lipid deposition and oxidative stress. This investigation indicates that EMF may be a novel therapeutic method for NAFLD.

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