NLRC4 inflammasome activation regulated by TNF-α promotes inflammatory responses in nonalcoholic fatty liver disease

2019 ◽  
Vol 511 (3) ◽  
pp. 524-530 ◽  
Author(s):  
Yihe Chen ◽  
Kuifen Ma
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Inflammatory Responses ◽  
Inflammasome Activation ◽  
Nonalcoholic Fatty Liver ◽  
Tnf Α

scholarly journals Effect of dietary intervention, with or without co-interventions, on inflammatory markers in patients with nonalcoholic fatty liver disease: a systematic literature review

2019 ◽  
Vol 77 (11) ◽  
pp. 765-786 ◽  
Author(s):  
Anjana J Reddy ◽  
Elena S George ◽  
Stuart K Roberts ◽  
Audrey C Tierney
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Inflammatory Markers ◽  
Fatty Liver Disease ◽  
Dietary Intervention ◽  
Cochrane Library ◽  
Dietary Interventions ◽  
Nonalcoholic Fatty Liver ◽  
Tnf Α

Abstract Context Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of liver disorders, ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), with inflammation acting as a key driver in its pathogenesis and progression. Diet has the potential to mediate the release of inflammatory markers; however, little is known about the effects of various diets. Objective This systematic review aimed to evaluate the effect of dietary interventions on cytokines and adipokines in patients with NAFLD. Data Sources The electronic databases MEDLINE, EMBASE, CINAHL, and Cochrane Library were searched for clinical trials investigating dietary interventions, with or without supplementation, on cytokines and adipokines in NAFLD patients. Data Extraction Basic characteristics of populations, dietary intervention protocol, cytokines, and adipokines were extracted for each study. Quality of evidence was assessed using the American Dietetic Association criteria. Data Analysis Nineteen studies with a total of 874 participants were included. The most frequently reported inflammatory outcomes were C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), adiponectin, and leptin. Hypocaloric, isocaloric, or low-fat diets significantly (P < 0.05) lowered levels of CRP, TNF-α, and adiponectin. The addition of nutraceutical or pharmacological supplementation to dietary interventions appeared to elicit additional benefits for all of the most frequently reported inflammatory markers. Conclusions Hypo- or isocaloric diets alone, or with co-interventions that included a nutraceutical or pharmacological supplementation, appear to improve the inflammatory profile in patients with NAFLD. Thus, anti-inflammatory diets may have the potential to improve underlying chronic inflammation that underpins the pathophysiological mechanisms of NAFLD. In the absence of any known liver-sensitive markers, the use of cytokines and adipokines as a surrogate marker of liver disease should be further investigated in well-controlled trials.

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 Prevalence of nonalcoholic fatty liver disease (NAFLD) in patients of cardiovascular diseases and its association with hs-CRP and TNF-α

2014 ◽  
Vol 66 (6) ◽  
pp. 574-579 ◽  
Author(s):  
Masihur Rehman Ajmal ◽  
Monika Yaccha ◽  
Mohammed Azharuddin Malik ◽  
M.U. Rabbani ◽  
Ibne Ahmad ◽  
...  
Keyword(s):  
Liver Disease ◽  
Cardiovascular Diseases ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Tnf Α ◽  
Hs Crp

Macrophages in Nonalcoholic Fatty Liver Disease: A Role Model of Pathogenic Immunometabolism

2017 ◽  
Vol 37 (03) ◽  
pp. 189-197 ◽  
Author(s):  
Oliver Krenkel ◽  
Frank Tacke
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Role Model ◽  
Inflammatory Responses ◽  
Macrophage Polarization ◽  
Nonalcoholic Fatty Liver ◽  
Inflammatory Stimuli ◽  
Functional Polarization

AbstractNonalcoholic fatty liver disease (NAFLD) and its progressive inflammatory form, nonalcoholic steatohepatitis (NASH), are leading causes of liver cirrhosis and hepatocellular carcinoma. Metabolism and inflammation are intimately interrelated in NAFLD/NASH, as expressed by the term immunometabolism. Hepatic macrophages mediate inflammatory responses during metabolic disorders and can stimulate or dismantle liver fibrosis. Their functional diversity is partly explained by heterogeneous macrophage subsets: tissue-resident Kupffer cells and monocyte-derived macrophages. However, macrophages themselves are altered in their functional polarization by dietary composition and metabolic or inflammatory stimuli in NAFLD. The inflammatory polarization of macrophages correlates with changes in core metabolism pathways like oxidative phosphorylation and glycolysis. The availability of nutrients, such as glucose or fatty acids or oxygen also influences macrophage polarization upon danger signal or cytokine reception. Understanding the interplay of metabolism and macrophage function in NASH may open new approaches to therapeutic targeting of these essential modifiers in metabolic liver diseases.

scholarly journals Ginseng Saponin Enriched in Rh1 and Rg2 Ameliorates Nonalcoholic Fatty Liver Disease by Inhibiting Inflammasome Activation

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 856
Author(s):  
Feng Wang ◽  
Jeong-Su Park ◽  
Yuanqiang Ma ◽  
Hwan Ma ◽  
Yeo-Jin Lee ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fast Food ◽  
Fatty Liver Disease ◽  
Inflammasome Activation ◽  
Nonalcoholic Fatty Liver ◽  
Ginseng Saponin ◽  
Pharmacologically Active

Nonalcoholic fatty liver disease (NAFLD) is becoming one of the most common chronic liver diseases in the world. One of the features of NAFLD is hepatic fat accumulation, which further causes hepatic steatosis, fibrosis, and inflammation. Saponins, the major pharmacologically active ingredients isolated from Panax notoginseng, contain several ginsenosides, which have various pharmacological and therapeutic functions. However, the ginsenoside-specific molecular mechanism of saponins in NAFLD remains unknown. This study aimed to elucidate the effects of ginseng saponin extract and its ginsenosides on hepatic steatosis, fibrosis, and inflammation and their underlying action mechanism in NAFLD. Mice were fed a fast food diet (FFD) for 16 weeks to induce NAFLD and then treated with saponin extract (50 or 150 mg/kg) for the remaining nine weeks to determine the effects of saponin on NAFLD. Saponin extract administration significantly alleviated FFD-induced hepatic steatosis, fibrosis, and inflammation. Particularly, saponin extract, compared with conventional red ginseng, contained significantly increased amounts of ginsenosides (Rh1 (10.34-fold) and Rg2 (7.1-fold)). In vitro Rh1 and Rg2 treatments exerted an anti-steatotic effect in primary hepatocytes, an antifibrotic effect in hepatic stellate cells, and anti-inflammatory and pro-mitophagy effects in immortalized mouse Kupffer cells. Mechanistically, saponin extract alleviated lipopolysaccharide-induced NLRP3 inflammasome activation by promoting mitophagy. In conclusion, saponin extract inhibited inflammation-mediated pathological inflammasome activation in macrophages, thereby preventing NAFLD development. Thus, saponin extract administration may be an alternative method for NAFLD prevention.

Simultaneous co-assembly of fenofibrate and ketoprofen peptide for the dual-targeted treatment of nonalcoholic fatty liver disease (NAFLD)

2020 ◽  
Vol 56 (36) ◽  
pp. 4922-4925 ◽  
Author(s):  
Zhongyan Wang ◽  
Chuanrui Ma ◽  
Yuna Shang ◽  
Lijun Yang ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Inflammatory Responses ◽  
Targeted Treatment ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

An ingenious co-assembled nanosystem based on fenofibrate and ketoprofen peptide for the dual-targeted treatment of NAFLD by reducing hepatic lipid accumulation and inflammatory responses.

scholarly journals Impact of the Co-Administration of N-3 Fatty Acids and Olive Oil Components in Preclinical Nonalcoholic Fatty Liver Disease Models: A Mechanistic View

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 499 ◽  
Author(s):  
Rodrigo Valenzuela ◽  
Luis A. Videla
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Olive Oil ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Liver Steatosis ◽  
Virgin Olive Oil ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is present in approximately 25% of the population worldwide. It is characterized by the accumulation of triacylglycerol in the liver, which can progress to steatohepatitis with different degrees of fibrosis, stages that lack approved pharmacological therapies and represent an indication for liver transplantation with consistently increasing frequency. In view that hepatic steatosis is a reversible condition, effective strategies preventing disease progression were addressed using combinations of natural products in the preclinical high-fat diet (HFD) protocol (60% of fat for 12 weeks). Among them, eicosapentaenoic acid (C20:5n-3, EPA) and docosahexaenoic acid (C22:5n-3, DHA), DHA and extra virgin olive oil (EVOO), or EPA plus hydroxytyrosol (HT) attained 66% to 83% diminution in HFD-induced steatosis, with the concomitant inhibition of the proinflammatory state associated with steatosis. These supplementations trigger different molecular mechanisms that modify antioxidant, antisteatotic, and anti-inflammatory responses, and in the case of DHA and HT co-administration, prevent NAFLD. It is concluded that future studies in NAFLD patients using combined supplementations such as DHA plus HT are warranted to prevent liver steatosis, thus avoiding its progression into more unmanageable stages of the disease.

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