scholarly journals Oxidative stress-induced growth inhibitor 1 in alcohol-induced liver cirrhosis

Author(s):  
Jarosław Sak ◽  
Andrzej Prystupa ◽  
Hanna Bis-Wencel ◽  
Paweł Kiciński ◽  
Dorota Luchowska-Kocot ◽  
...  
2016 ◽  
Vol 15 (3) ◽  
pp. 402-409 ◽  
Author(s):  
Kirsten E. Pijls ◽  
Daisy M.A.E. Jonkers ◽  
Montserrat Elizalde ◽  
Marie-Jose Drittij-Reijnders ◽  
Guido R. Haenen ◽  
...  

2021 ◽  
Vol 14 (1) ◽  
pp. 123-131
Author(s):  
Doha M. Beltagy ◽  
Khloud Gamal Abdelsalam ◽  
Tarek M Mohamed ◽  
Mai M. El-Keey

Liver cirrhosis is currently the 11th most common cause of death which includes inflammatory, oxidative damage, and immune response. Harmaline has antioxidant and anti-inflammatory mechanisms which can defeat against hepatic cirrhosis pathways. The present work aimed to evaluate the ameliorating effect of harmaline against liver cirrhosis induced by thioacetamide in mice. The study was carried out on sixty male mice divided into three main groups. Control and harmaline groups (GIa and GIb), thioacetamide-group (GII) and harmaline co-treated and treated groups (GIIIa and GIIIb). By the end of the experiment, adiponectin concentrations were measured in serum and liver tissue. Gene expression of adiponectin, transforming growth factor beta-1 (TGF-β1), tissue inhibitor metalloprotease-1(TIMP-1) and peroxisome proliferator activated receptor-gamma (PPAR-γ) were assessed. Some oxidative stress biomarkers as malondialdehyde, reduced glutathione, catalase, superoxide dismutase and nitric oxide were determined. The results indicated that harmaline administration cause significant suppression of oxidative stress and inflammatory response.Inhibition of hepatic stellate cell activation and extracellular matrix deposition were also noticed with a significant decrease in the expression of the profibrotic markers(TGF-β1 and TIMP-1) which have direct effects on adiponectin activation. These results were confirmed by the histological studies in liver tissue. In Conclusion,Harmaline has excellent protective role against liver cirrhosis induced by thioacetamide in mice via its antioxidant and anti-inflammatory properties.It can be therapeutically used as a safe liver support by a dose of 10 mg/kg after furtherin vivo studies.


2006 ◽  
Vol 202 (11) ◽  
pp. 777-788 ◽  
Author(s):  
Peng Lv ◽  
He-Sheng Luo ◽  
Xiao-Ping Zhou ◽  
Shelley Chireyath Paul ◽  
Yan-Jv Xiao ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1978
Author(s):  
Chia-Yu Lai ◽  
Shao-Bin Cheng ◽  
Teng-Yu Lee ◽  
Yung-Fang Hsiao ◽  
Hsiao-Tien Liu ◽  
...  

Vitamin B-6 and glutathione (GSH) are antioxidant nutrients, and inadequate vitamin B-6 may indirectly limit glutathione synthesis and further affect the antioxidant capacities. Since liver cirrhosis is often associated with increased oxidative stress and decreased antioxidant capacities, we conducted a double-blind randomized controlled trial to assess the antioxidative effect of vitamin B-6, GSH, or vitamin B-6/GSH combined supplementation in cirrhotic patients. We followed patients after the end of supplementation to evaluate the association of vitamin B-6 and GSH with disease severity. In total, 61 liver cirrhosis patients were randomly assigned to placebo, vitamin B-6 (50 mg pyridoxine/d), GSH (500 mg/d), or B-6 + GSH groups for 12 weeks. After the end of supplementation, the condition of patient’s disease severity was followed until the end of the study. Neither vitamin B-6 nor GSH supplementation had significant effects on indicators of oxidative stress and antioxidant capacities. The median follow-up time was 984 d, and 21 patients were lost to follow-up. High levels of GSH, a high GSH/oxidized GSH ratio, and high GSH-St activity at baseline (Week 0) had a significant effect on low Child–Turcotte–Pugh scores at Week 0, the end of supplementation (Week 12), and the end of follow-up in all patients after adjusting for potential confounders. Although the decreased GSH and its related enzyme activity were associated with the severity of liver cirrhosis, vitamin B-6 and GSH supplementation had no significant effect on reducing oxidative stress and increasing antioxidant capacities.


2017 ◽  
Vol 8 (1) ◽  
pp. 397-405 ◽  
Author(s):  
Yi-Ju Lee ◽  
Jeng-Dong Hsu ◽  
Wea-Lung Lin ◽  
Shao-Hsuan Kao ◽  
Chau-Jong Wang

Excessive alcohol uptake exerts hepatocellular toxicity, ultimately leading to multiple liver diseases such as steatohepatitis and liver cirrhosis.


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Marina Galicia-Moreno ◽  
Dorothy Rosique-Oramas ◽  
Zaira Medina-Avila ◽  
Tania Álvarez-Torres ◽  
Dalia Falcón ◽  
...  

Alcohol is the most socially accepted addictive substance worldwide, and its metabolism is related with oxidative stress generation. The aim of this work was to evaluate the role of oxidative stress in alcoholic liver cirrhosis (ALC). This study included 187 patients divided into two groups: ALC, classified according to Child-Pugh score, and a control group. We determined the levels of reduced and oxidized glutathione (GSH and GSSG) and the GSH/GSSG ratio by an enzymatic method in blood. Also, protein carbonyl and malondialdehyde (MDA) content were estimated in serum. MDA levels increased in proportion to the severity of damage, whereas the GSH and GSSG levels decreased and increased, respectively, at different stages of cirrhosis. There were no differences in the GSH/GSSG ratio and carbonylated protein content between groups. We also evaluated whether the active consumption of or abstinence from alcoholic beverages affected the behavior of these oxidative markers and only found differences in the MDA, GSH, and GSSG determination and the GSH/GSSG ratio. Our results suggest that alcoholic cirrhotic subjects have an increase in oxidative stress in the early stages of disease severity and that abstinence from alcohol consumption favors the major antioxidant endogen: GSH in patients with advanced disease severity.


2012 ◽  
Vol 56 ◽  
pp. S234
Author(s):  
V. Raparelli ◽  
L. Napoleone ◽  
O. Riggio ◽  
M. Merli ◽  
F. Angelico ◽  
...  

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