scholarly journals Quantitative Profiling of Oxylipin Reveals the Mechanism of Pien-Tze-Huang on Alcoholic Liver Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Ziye Zhu ◽  
Wenjun Zhou ◽  
Yang Yang ◽  
Kai Wang ◽  
Fenghua Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Hepatic Steatosis ◽  
Alcoholic Liver Disease ◽  
Liver Steatosis ◽  
Normal Diet ◽  
Eicosatetraenoic Acid ◽  
Control Group ◽  
Pien Tze Huang ◽  
Commercial Kits

Alcoholic liver disease (ALD) is a liver disease caused by long-term alcohol consumption. ROS-mediated oxidative stress is the leading cause of ALD. Pien-Tze-Huang (PZH), a traditional formula, is famous in China. This study was designed to evaluate the effects and explore the potential mechanisms of PZH in ALD. Forty mice were randomly divided into five groups: control group (normal diet + vehicle), model group (ethanol diet + vehicle), PZH-L group (ethanol diet + PZH (0.125 g/kg)), PZH-M group (ethanol diet + PZH (0.25 g/kg)), and PZH-H group (ethanol diet + PZH (0.5 g/kg)). The mice were sacrificed, and their liver and blood samples were preserved. Liver steatosis, triglyceride (TG), total cholesterol, serum alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were assayed. Malondialdehyde (MDA), glutathione peroxidase (GSH-PX), and total superoxide dismutase were identified using commercial kits. Oxylipins were profiled, and the data were analyzed. The AMPK/ACC/CPT1A pathway was identified using real-time polymerase chain reaction and western blotting. The PZH-H intervention significantly alleviated hepatic steatosis and injury and reduced the levels of liver TG and serum ALT and AST. In addition, MDA levels were markedly reduced, and GSH-PX activity significantly increased after PZH-H intervention. Finally, PZH-H increased the levels of 17-HETE, 15-HEPE, 9-HOTrE, 13-HOTrE, and 5,6-dihydroxy-8Z,11Z,14Z,17Z-eicosatetraenoic acid, and reduced PGE2 levels. PZH-H intervention also promoted the phosphorylation of AMPK and ACC, and the expression of CPT1A. In conclusion, PZH reduced oxidative stress and alleviated hepatic steatosis and injury. The mechanism was correlated with the oxylipin metabolites/AMPK/ACC/CPT1A axis.

scholarly journals Protective effect of apricot (Prunus armeniacaL.) on hepatic steatosis and damage induced by carbon tetrachloride in Wistar rats

2009 ◽  
Vol 102 (12) ◽  
pp. 1767-1775 ◽  
Author(s):  
Feral Ozturk ◽  
Mehmet Gul ◽  
Burhan Ates ◽  
I. Cetin Ozturk ◽  
Asli Cetin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Hepatic Steatosis ◽  
Wistar Rats ◽  
Liver Steatosis ◽  
Radical Scavenging ◽  
Hepatic Necrosis ◽  
Control Group ◽  
Cytoplasmic Matrix

The present study was planned to investigate the protective effect of 10 % and 20 % apricot-containing feed on carbon tetrachloride (CCl4)-induced hepatic steatosis and damage. Adult male Wistar rats (n42) were divided into six groups of seven each, as follows: control group; CCl4group; CCl4+10 % apricot group; CCl4+20 % apricot group; 10 % apricot group; 20 % apricot group. All apricot groups were fed with 10 % or 20 % apricot-containing feed for 5 months. CCl4injections were applied to the CCl4groups at the dose of 1 mg/kg for 3 d at the end of 5 months. In the CCl4group, vacuolated hepatocytes and hepatic necrosis were seen, especially in the centrilobular area. Hepatocytes showed an oedematous cytoplasmic matrix, large lipid globules and degenerated organelles. The area of liver injury was found significantly decreased with apricot feeding. Malondialdehyde and total glutathione levels and catalase, superoxide dismutase and glutathione peroxidase activities were significantly changed in the CCl4group and indicated increased oxidative stress. Apricot feeding decreased this oxidative stress and ameliorated histological damage. We concluded that apricot feeding had beneficial effects on CCl4-induced liver steatosis and damage probably due to its antioxidant nutrient (β-carotene and vitamin) contents and high radical-scavenging capacity. Dietary intake of apricot can reduce the risk of liver steatosis and damage caused by free radicals.

scholarly journals Hepatocellular damage and inflammation in various forms of alcoholic liver disease

2021 ◽  
Vol 93 (1) ◽  
pp. 15-19
Author(s):  
Alisa S. Rodina ◽  
Marina E. Shubina ◽  
Irina V. Kurbatova ◽  
Ludmila V. Topchieva ◽  
Olga P. Dudanova
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Clinical Laboratory ◽  
Cell Damage ◽  
Liver Steatosis ◽  
Hepatic Cell ◽  
Control Group ◽  
Healthy Individuals ◽  
Hepatocellular Damage ◽  
Immune Inflammation

Aim. The aim of the study was to evaluate hepatocellular damage and immune inflammation in various forms of alcoholic liver disease (ALD). Materials and methods. 104 patients with ALD were examined: 15 (14.4%) with liver steatosis (LS), 19 (18.3%) with steatohepatitis and 70 (67.3%) with liver cirrhosis (LC); men 50 (48.1%), women 54 (51.9%); age 45.78.4 years. Traditional clinical, laboratory, instrumental studies were performed, the levels of fragments of cytokeratin-18 (FCK-18), cytokines IL-1, TNF-, IL-4, IL-6, IL-8 were determined by ELISA. The control group consisted of 39 healthy individuals: men 20 (51.2%), women 19 (48.7%), age 48.58.3 years. Results. In LS, an increase in the level of FCK-18 was noted with normal aminotransferase activity, the content of TNF-, IL-6, IL-1, IL-8 increased and the level of IL-4 decreased compared to those in healthy individuals. In steatohepatitis, a triple increase in aminotransferases and FCK-18 was observed compared with LS, as well as an increase in the level of inflammatory mediators, to a greater extent IL-6, to a lesser extent IL-8, TNF-, a decrease in IL-4, IL-1 remained at the same level. In LC, there was a further increase in FCK-18, significantly more pronounced than an increase in AST, and the increase in cytokines continued to the same extent, the levels of IL-6 and IL-8, to a lesser extent IL-1 and TNF-, and the level of IL-4. Conclusion. With the progression of ALD from LS to steatohepatitis, hepatic cell damage was carried out by equally pronounced processes of hepatocyte necrosis and apoptosis, with the development of cirrhosis of the liver, parenchyma damage occurred mainly due to hepatocyte apoptosis. The immuno-inflammatory process progressively increased from the stage of LS to LC with IL-6 and IL-8 undergoing the greatest dynamics. FCK-18 can serve as a non-invasive marker of hepatic cell damage, and IL-6 and IL-8 markers of immune inflammation in ALD.

A polysaccharide of PFP-1 from Pleurotus geesteranus attenuates alcoholic liver diseases via Nrf2 and NF-κB signaling pathways

2021 ◽  
Author(s):  
Xinling Song ◽  
Wenxue Sun ◽  
Wenxin Cai ◽  
Le Jia ◽  
Jianjun Zhang
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Liver Injury ◽  
Signaling Pathways ◽  
Alcoholic Liver Disease ◽  
Fruiting Body ◽  
Liver Diseases ◽  
Alcoholic Liver Diseases

A polysaccharide named as PFP-1 was isolated from Pleurotus geesteranus fruiting body, and the potential investigations on ameliorating oxidative stress and liver injury against alcoholic liver disease (ALD) were processed...

Metabolism of vitamin D in patients with primary biliary cirrhosis and alcoholic liver disease

1985 ◽  
Vol 69 (5) ◽  
pp. 561-570 ◽  
Author(s):  
E. Barbara Mawer ◽  
H. J. Klass ◽  
T. W. Warnes ◽  
Jacqueline L. Berry
Keyword(s):  
Vitamin D ◽  
Liver Disease ◽  
Primary Biliary Cirrhosis ◽  
Alcoholic Liver Disease ◽  
Vitamin D3 ◽  
Control Group ◽  
Biliary Cirrhosis ◽  
Vitamin D2 ◽  
Dihydroxyvitamin D3 ◽  
Poor Renal Function

1. The metabolism of isotopically labelled vitamin D2 and D3 has been investigated in eight patients with primary biliary cirrhosis and in five controls. The concentration of labelled vitamin D2 was lower than that of vitamin D3 in serum of patients with primary biliary cirrhosis on days 1 and 2 after intravenous injection (P < 0.005 and P < 0.05, respectively) but no difference was seen in controls. 2. Similar amounts of labelled 25-hydroxyvitamin D2 and D3 were seen in serum of the control group; the same pattern was observed in the primary biliary cirrhosis group, and no significant differences were observed between the two groups. 3. In both control and primary biliary cirrhosis groups, the serum concentration of labelled 24,25-dihydroxyvitamin D2 exceeded that of 24,25-dihydroxyvitamin D3 (significant for controls on day 2, P < 0.02) but concentrations in the two groups were not different. 4. Concentrations of labelled 25,26-dihydroxyvitamin D3 were significantly higher than those of 25,26-dihydroxyvitamin D2 in the primary biliary cirrhosis group at all times and in the control group on days 2 and 3. Both 25,26-dihydroxyvitamin D2 and D3 were higher in the serum of patients with primary biliary cirrhosis than in controls (significant on day 1, P < 0.05). 5. Urinary excretion over days 0–3 of radioactivity from both vitamins D2 and D3 was significantly higher in the primary biliary cirrhosis group than in controls: 12.03 vs 1.80% for vitamin D2 and 8.98 vs 1.76% for vitamin D3(P < 0.005). Vitamin D2-derived urinary radioactivity in primary biliary cirrhosis correlated strongly with serum bilirubin (P = 0.005). 6. The metabolism of labelled vitamin D3 was studied in seven patients with alcoholic liver disease, three of whom showed low serum concentrations of labelled 25-hydroxyvitamin D3 suggesting impaired hepatic synthesis. The 25-hydroxylation response was quantified as the relative index of 25-hydroxylation and was significantly related to two other indices of liver function. It is concluded that impaired 25-hydroxylation of vitamin D may occur in alcoholic liver disease and results from hepatocellular dysfunction. 7. Less than the predicted amounts of 1,25-dihydroxyvitamin D3 were produced in four of the seven patients with alcoholic liver disease; this defect may be attributable in part to decreased precursor 25-hydroxyvitamin D and to poor renal function.

Relationship of serum vaspin, nafld fibrosis score to ultrasonographic detection and quantification of steatosis in nonalcoholic fatty liver disease patients

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Essam Mohamed Byoumy ◽  
Moataz Mohamed Sayed ◽  
Shereen Abo Baker Abd El-Rahman ◽  
Sara Abd Elkader Al-Nakib ◽  
Mohamed Magdy Salama ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Steatosis ◽  
Control Group ◽  
P Value ◽  
Fibrosis Score ◽  
Alcoholic Fatty Liver ◽  
Nafld Fibrosis Score ◽  
Detection And Quantification

Abstract Background Ectopic hepatic lipid accumulation is closely related to the development of insulin resistance, which is regarded as one of the most significant risk factors of non-alcoholic fatty liver disease (NAFLD). The aim of the study was to evaluate and validate the diagnostic value of serum vaspin, NAFLD Fibrosis Score and sonograghic parameters in detection and quantification of liver steatosis and determining further need for liver biopsy or other means to establish NAFLD diagnosis. Methods This study was carried out on 60 patients having bright liver in ultrasonography and 30 healthy persons as controls. The subjects were divided into the following groups; group A: 30 age and sex matched healthy volunteers (control group), group B: 20 patients with fatty liver grade I, group C: 20 patients with fatty liver grade II and group D: 20 patients with fatty liver grade III. Results serum vaspine levels and NAFLD fibrosis score, were significantly higher in patients than in controls with p-value:&lt;0.001. There was a significant positive correlation between NAFLD fibrosis score and serum vaspin and ultrasonographic findngs of NAFLD with p-value: &lt;0.001. Conclusion Vaspin seem to be the most suitable non-invasive biomarker in predicting both intrahepatic lipid contents in NAFLD group.

scholarly journals Crosstalk between Oxidative Stress and Inflammatory Liver Injury in the Pathogenesis of Alcoholic Liver Disease

2022 ◽  
Vol 23 (2) ◽  
pp. 774
Author(s):  
Yoon Mee Yang ◽  
Ye Eun Cho ◽  
Seonghwan Hwang
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Pathological Features ◽  
Excessive Alcohol Consumption ◽  
Excessive Alcohol ◽  
The Relationship

Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed to elucidate pathological features and pathogenic mechanisms underlying ALD. Notably, oxidative changes in the liver have been recognized as a signature trait of ALD. Progression of ALD is linked to the generation of highly reactive free radicals by reactions involving ethanol and its metabolites. Furthermore, hepatic oxidative stress promotes tissue injury and, in turn, stimulates inflammatory responses in the liver, forming a pathological loop that promotes the progression of ALD. Accordingly, accumulating further knowledge on the relationship between oxidative stress and inflammation may help establish a viable therapeutic approach for treating ALD.

scholarly journals The role of brief intervention in achieving and maintaining abstinence in patients with alcoholic liver disease

2020 ◽  
pp. 182-188
Author(s):  
V. D. Lunkov ◽  
M. V. Maevskaya ◽  
V. T. Ivashkin
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Psychological Intervention ◽  
Decompensated Cirrhosis ◽  
Control Group ◽  
Factors Associated ◽  
Entire Observation Period ◽  
Group A ◽  
Observation Period

Objective of the study. prove the effectiveness of brief psychological intervention (BPI) conducted by an internist in achieving and maintaining abstinence in patients with alcoholic liver disease (ALD).Materials and methods. A total of 65 patients were included in the study: 29 patients in the BPI group and 36 in the historical control group. A comparative analysis of the frequency of achievement and maintenance of abstinence and analysis of factors associated with these parameters were conducted.Results of the study. The frequency of achieving abstinence was significantly higher in the BPI group compared with the control group after 6, 9, 12 and 24 months from the date of inclusion in the study (p <0.001, p = 0.002, p = 0.001, p = 0.017, respectively; criterion χ2). The frequency of failures to achieve abstinence in the CPC group was significantly lower than in the control group after 6 months and in general for the entire observation period (p = 0.004, p = 0.005, respectively; criterion χ2). Provision of BPIs for 12 months after alcohol-induced decompensation serves as a factor that is reliably associated with achieving total abstinence within 24 months (p = 0.001, criterion χ2). Decompensated cirrhosis of the liver serves as factors independently associated with failures to achieve abstinence within 24 months after alcohol-induced illness (OS: 10.72 [95% CI 2.17–52.81]; p = 0.004) and the absence of BPI after discharge from the hospital (OSH BPI: 0.80 [95% CI 0.14–0.479]; p = 0.006)Conclusion. BPIs provided by an internist to the patients with ABD for 12 months after alcohol-induced decompensation leads to a higher rate of achieving total abstinence and decrease in the frequency of failures to achieve abstinence within 24 months after discharge from the hospital.

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