Polysaccharides Attenuate Alcohol-Induced Liver Damage by Regulating Fatty Acid Synthesis, Degradation and Glycerophospholipid Metabolism in Mice.

Front Pharmacol

Key Laboratory for Information System of Mountainous Areas and Protection of Ecological Environment, Guizhou Normal University, Guiyang, China.

Published: October 2021

polysaccharides (MFP) are macromolecules extracted from Mori Fructus (MF), which has the biological activity of anti-liver damage. Our group found that MFP maybe down regulate the serum triglyceride level in mice with alcohol-induced liver damage, suggesting that MFP can regulate lipid metabolism, but its specific mechanism is still not clear. Fifty SPF-ICR male mice weighing 18-22 g were randomly divided into five groups, blank group, model group, bifendate group, MFPA1 group and MFPB1 group. The blood and liver tissues were taken from mice for nontargeted lipidomic analysis and histopathological examination after 7 day's treatment. The histopathological changes indicated that the normal liver cells were intact and regular, with orderly arrangement and distinct cell boundaries; the liver of model mice showed inflammatory infiltration, ballooning degeneration in the cells and small lipid drops; the liver of mice in the bifendate, MFPA1 and MFPB1 groups showed similar symptoms to those of model mice, but the lesions were less severe and the ballooning degeneration were reduced. Multivariate analysis of all lipids in the serum of five groups of mice showed there were obvious differences in lipid metabolism between the model group and the blank group. At the same time, seven kinds of differential lipids were precisely identified after screening, including prostaglandins, long-chain fatty acids, glycerophospholipids, acyl carnitines. In summary, alcohol intake and MFP intervention have significant effects on fatty acid synthesis, degradation and glycerophospholipid metabolism.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8569108PMC
http://dx.doi.org/10.3389/fphar.2021.766737DOI Listing

Publication Analysis

Top Keywords

alcohol-induced liver
8
liver damage
8
fatty acid
8
acid synthesis
8
synthesis degradation
8
degradation glycerophospholipid
8
glycerophospholipid metabolism
8
mice
8
group
8
mfp regulate
8

Similar Publications

Post-COVID metabolic enzyme alterations in K18-hACE2 mice exacerbate alcohol-induced liver injury through transcriptional regulation.

Free Radic Biol Med

January 2025

Korea Mouse Phenotyping Center, Seoul National University, Seoul 08826, Republic of Korea; Laboratory of Developmental Biology and Genomics, Research Institute for Veterinary Science, and BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, Seoul National University, Seoul 08826, Republic of Korea; Interdisciplinary Program for Bioinformatics, Program for Cancer Biology and BIO-MAX/N-Bio Institute, Seoul National University, Seoul 08826, Republic of Korea. Electronic address:

Article Synopsis
  • COVID-19, caused by SARS-CoV-2, poses serious global health risks, including the potential for secondary liver injury related to metabolic enzyme changes.
  • This study explores how prior infection with SARS-CoV-2 affects alcohol-induced liver damage, using transgenic mice that express human ACE2.
  • Results showed that infected mice experienced worsened liver injury after alcohol consumption, with alterations in metabolic enzymes and increased levels of a toxic alcohol byproduct, indicating a complex interaction between COVID-19 and alcohol effects on the liver.
View Article and Find Full Text PDF

The Effects of Moderate to High Static Magnetic Fields on Pancreatic Damage.

J Magn Reson Imaging

January 2025

High Magnetic Field Laboratory, CAS Key Laboratory of High Magnetic Field and Ion Beam Physical Biology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, China.

Background: Pancreatic damage is a common digestive system disease with no specific drugs. Static magnetic field (SMF), the key component of magnetic resonance imaging (MRI), has demonstrated prominent effects in various disease models.

Purpose: To study the effects of 0.

View Article and Find Full Text PDF

Alcohol-related liver disease (ALD) is a serious global health concern, characterized by liver inflammation and progressive fibrosis. There are no Food and Drug Administration-approved drugs, thus effective treatments are needed. Severe alcoholic hepatitis (AH) is the most severe manifestation of ALD, with a 28-day mortality rate ranging from 20% to 50%.

View Article and Find Full Text PDF

This study demonstrates the effectiveness of propidium iodide as a reliable marker for detecting dead or dying cells in frozen liver tissue sections. By comparing propidium iodide staining with the widely used Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, both methods showed consistent results in disease models such as alcohol-induced fibrosis and Western diet-induced fatty liver. Additionally, propidium iodide was successfully co-stained with other fluorescent markers, like phalloidin (for actin filaments) and antibodies targeting collagen, enabling detailed spatial analysis of dying cells within tissue.

View Article and Find Full Text PDF
Article Synopsis
  • High-mobility group box-1 (HMGB1) levels rise and undergo post-translational modifications (PTMs) with alcohol consumption, potentially influencing the development of alcohol-associated liver disease (AALD).
  • Researchers used a specific model of liver injury caused by alcohol to explore how manipulating HMGB1's expression and modifications in liver cells and immune cells impacts AALD.
  • Their findings show that different forms of HMGB1 have contrasting effects: oxidized HMGB1 (O) worsens liver injury while acetylated HMGB1 (Ac) can protect against these harmful effects, highlighting the importance of targeting O HMGB1 in treating AALD.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!