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...

Significance of iron indices in hepatitis C, alcoholic liver disease, and non-C, non-alcoholic liver diseases

1995 ◽  
Vol 108 (4) ◽  
pp. A1075
Author(s):  
A.A. Gossard ◽  
J.B. Gross ◽  
L.J. Burgart ◽  
J.J. Poterucha ◽  
N.N. Zein
Keyword(s):  
Liver Disease ◽  
Hepatitis C ◽  
Alcoholic Liver Disease ◽  
Liver Diseases ◽  
Alcoholic Liver Diseases

scholarly journals INDICES OF OXIDATIVE STRESS AND LIVER INJURY IN ALCOHOLIC LIVER DISEASE

2017 ◽  
Vol 4 (5) ◽  
pp. 488-492
Author(s):  
Pinky Garg ◽  
◽  
Saroj Choudhary ◽  
Montosh Chakraborty ◽  
Karthikeyan P ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Liver Injury ◽  
Alcoholic Liver Disease

scholarly journals The Purinergic P2X7 Receptor-NLRP3 Inflammasome Pathway: A New Target in Alcoholic Liver Disease?

2021 ◽  
Vol 22 (4) ◽  
pp. 2139
Author(s):  
Brendan Le Daré ◽  
Pierre-Jean Ferron ◽  
Thomas Gicquel
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Kupffer Cells ◽  
Nlrp3 Inflammasome ◽  
Liver Diseases ◽  
Current Knowledge ◽  
Purinergic Signaling ◽  
World Health ◽  
Alcoholic Liver Diseases

The World Health Organization has estimated that approximately 3 million deaths are attributable to alcohol consumption each year. Alcohol consumption is notably associated with the development and/or progression of many non-communicable inflammatory diseases—particularly in the liver. Although these alcoholic liver diseases were initially thought to be caused by the toxicity of ethanol on hepatocytes, the latest research indicates Kupffer cells (the liver macrophages) are at the heart of this “inflammatory shift”. Purinergic signaling (notably through P2X7 receptors and the NLRP3 inflammasome) by Kupffer cells appears to be a decisive factor in the pathophysiology of alcoholic liver disease. Hence, the modulation of purinergic signaling might represent a new means of treating alcoholic liver disease. Here, we review current knowledge on the pathophysiology of alcoholic liver diseases and therapeutic perspectives for targeting these inflammatory pathways.

Three-spot seahorse-derived peptide PAGPRGPA attenuates ethanol-induced oxidative stress in LO2 cells through MAPKs, Keap1/Nrf2 signalling pathway and amino acid metabolism

2021 ◽  
Author(s):  
Jie Shi ◽  
Xin Zhou ◽  
Ying Zhao ◽  
Xuemei Tang ◽  
Lu Feng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Amino Acid ◽  
Global Health ◽  
Alcoholic Liver Disease ◽  
Liver Diseases ◽  
Amino Acid Metabolism ◽  
Bioactive Peptides ◽  
Acid Metabolism ◽  
Marine Organisms

Various types of liver diseases such as the alcoholic liver disease (ALD) are still global health problems. Bioactive peptides isolated from people, marine organisms, animals and plants have shown hepatoprotective...

scholarly journals Protective Role of Antioxidants in Alcoholic Liver Disease

Med Phoenix ◽  
2018 ◽  
Vol 3 (1) ◽  
pp. 75-88 ◽  
Author(s):  
Manoranjan Adak
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Liver Diseases ◽  
Animal Studies ◽  
Radical Scavenging ◽  
Natural Antioxidants ◽  
Protective Role ◽  
Alcoholic Beverages

 Excessive consumption of alcoholic beverages is a serious cause of liver disease worldwide. Any abnormality or dysfunction of the liver leads major impairment of the organ function, which in turn, influences the health of the individual. Alcoholic liver disease (ALD) includes fatty liver, hepatic inflammation, liver cirrhosis, fibrosis, alcoholic hepatitis and finally hepatocellular carcinoma. The metabolism of ethanol generates reactive oxygen species, which play a significant role in the deterioration of alcoholic liver disease. Oxidative stress has been considered as a conjoint pathological mechanism, and it contributes to initiation and progression of liver injury. Antioxidants, phytochemicals, such as polyphenols, regulate the expression of ALDassociated proteins and peptides, namely, catalase, superoxide dismutase, glutathione, glutathione peroxidase, and glutathione reductase. Application of antioxidants signifies a rational curative strategy to prevent and cure liver diseases involving oxidative stress. Although conclusions drawn from clinical studies remain uncertain, animal studies have revealed the promising in-vivo therapeutic effect of antioxidants on liver diseases. Natural antioxidants contained in edible or medicinal plants often possess strong antioxidant and free radical scavenging abilities as well as anti-inflammatory action, which are also supposed to be the basis of other bioactivities and health benefits. Med Phoenix. Vol. 3, Issue. 1, 2018, Page: 75-88                                                         

scholarly journals Heme Oxygenase-1 Induction by Cobalt Protoporphyrin Ameliorates Cholestatic Liver Disease in a Xenobiotic-Induced Murine Model

2021 ◽  
Vol 22 (15) ◽  
pp. 8253
Author(s):  
Jung-Yeon Kim ◽  
Yongmin Choi ◽  
Jaechan Leem ◽  
Jeong Eun Song
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Heme Oxygenase ◽  
Murine Model ◽  
Liver Diseases ◽  
Transforming Growth Factor ◽  
Heme Oxygenase 1 ◽  
Cholestatic Liver Disease ◽  
Hepatocyte Apoptosis ◽  
Cobalt Protoporphyrin

Cholestatic liver diseases can progress to end-stage liver disease and reduce patients’ quality of life. Although their underlying mechanisms are still incompletely elucidated, oxidative stress is considered to be a key contributor to these diseases. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that displays antioxidant action. It has been found that this enzyme plays a protective role against various inflammatory diseases. However, the role of HO-1 in cholestatic liver diseases has not yet been investigated. Here, we examined whether pharmacological induction of HO-1 by cobalt protoporphyrin (CoPP) ameliorates cholestatic liver injury. To this end, a murine model of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet feeding was used. Administration of CoPP ameliorated liver damage and cholestasis with HO-1 upregulation in DDC diet-fed mice. Induction of HO-1 by CoPP suppressed the DDC diet-induced oxidative stress and hepatocyte apoptosis. In addition, CoPP attenuated cytokine production and inflammatory cell infiltration. Furthermore, deposition of the extracellular matrix and expression of fibrosis-related genes after DDC feeding were also decreased by CoPP. HO-1 induction decreased the number of myofibroblasts and inhibited the transforming growth factor-β pathway. Altogether, these data suggest that the pharmacological induction of HO-1 ameliorates cholestatic liver disease by suppressing oxidative stress, hepatocyte apoptosis, and inflammation.

Protective effects of fucoidan against ethanol-induced liver injury through maintaining mitochondria function and mitophagy balance in rats.

2021 ◽  
Author(s):  
Huichao Zhao ◽  
Shuang Liu ◽  
Hui Zhao ◽  
Meilan Xue ◽  
Huaqi Zhang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Alcoholic Liver Disease ◽  
Therapeutic Strategy ◽  
Hepatic Lesion ◽  
Protective Effects ◽  
Regulatory Effects

For alcoholic liver disease (ALD), mitophagy was reported as a promising therapeutic strategy to alleviate the hepatic lesion elicited by ethanol. This study was to investigate the regulatory effects of...

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