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Mol Immunol ; 170: 60-75, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38626622

ABSTRACT

Liver diseases caused by viral infections, alcoholism, drugs, or chemical poisons are a significant health problem: Liver diseases are a leading contributor to mortality, with approximately 2 million deaths per year worldwide. Liver fibrosis, as a common liver disease characterized by excessive collagen deposition, is associated with high morbidity and mortality, and there is no effective treatment. Numerous studies have shown that the accumulation of mast cells (MCs) in the liver is closely associated with liver injury caused by a variety of factors. This study investigated the relationship between MCs and carbon tetrachloride (CCl4)-induced liver fibrosis in rats and the effects of the MC stabilizers sodium cromoglycate (SGC) and ketotifen (KET) on CCl4-induced liver fibrosis. The results showed that MCs were recruited or activated during CCl4-induced liver fibrosis. Coadministration of SCG or KET alleviated the liver fibrosis by decreasing SCF/c-kit expression, inhibiting the TGF-ß1/Smad2/3 pathway, depressing the HIF-1a/VEGF pathway, activating Nrf2/HO-1 pathway, and increasing the hepatic levels of GSH, GSH-Px, and GR, thereby reducing hepatic oxidative stress. Collectively, recruitment or activation of MCs is linked to liver fibrosis and the stabilization of MCs may provide a new approach to the prevention of liver fibrosis.


Subject(s)
Carbon Tetrachloride , Cromolyn Sodium , Liver Cirrhosis , Liver , Mast Cells , Animals , Mast Cells/metabolism , Mast Cells/immunology , Mast Cells/drug effects , Carbon Tetrachloride/toxicity , Rats , Male , Liver Cirrhosis/metabolism , Liver Cirrhosis/pathology , Liver Cirrhosis/immunology , Liver Cirrhosis/chemically induced , Cromolyn Sodium/pharmacology , Liver/pathology , Liver/metabolism , Liver/drug effects , Transforming Growth Factor beta1/metabolism , Rats, Sprague-Dawley , Ketotifen/pharmacology , Chemical and Drug Induced Liver Injury/metabolism , Chemical and Drug Induced Liver Injury/pathology , Chemical and Drug Induced Liver Injury/immunology , Oxidative Stress/drug effects , NF-E2-Related Factor 2/metabolism , Signal Transduction/drug effects , Smad2 Protein/metabolism , Smad3 Protein/metabolism , Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Vascular Endothelial Growth Factor A/metabolism
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