ArticleExperimental and molecular pathology2011
S-adenosylmethionine prevents the up regulation of Toll-like receptor (TLR) signaling caused by chronic ethanol feeding in rats.
Article in Experimental and molecular pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Methionine Adenosyltransferase 1A and S-Adenosylmethionine in Alcohol-Associated Liver Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Alcohol: basic and translational research; 15th annual Charles Lieber &1st Samuel French satellite symposium.Experimental and molecular pathology · 2022Review
- Article
- Alcohol, aging, and innate immunity.Journal of leukocyte biology · 2017Review
- NOX2 amplifies acetaldehyde-mediated cardiomyocyte mitochondrial dysfunction in alcoholic cardiomyopathy.Scientific reports · 2016Article
- Protective Effects of S-Adenosylmethionine and Its Combinations With Taurine and/or Betaine Against Lipopolysaccharide or Polyinosinic-polycytidylic Acid-induced Acute Hepatotoxicity.Journal of cancer prevention · 2016Article
- The Role of Innate Immunity in Alcoholic Liver Disease.Alcohol research : current reviews · 2015Review
- Gut microbiota in alcoholic liver disease: pathogenetic role and therapeutic perspectives.World journal of gastroenterology · 2014Review
- New advances in molecular mechanisms and emerging therapeutic targets in alcoholic liver diseases.World journal of gastroenterology · 2014Review
- S-Adenosylmethionine attenuates lipopolysaccharide-induced liver injury by downregulating the Toll-like receptor 4 signal in Kupffer cells.Hepatology international · 2014Article
- The liver is populated by a broad spectrum of markers for macrophages. In alcoholic hepatitis the macrophages are M1 and M2.Experimental and molecular pathology · 2014Article
- Balloon liver cells forming Mallory-Denk-bodies are progenitor cells.Experimental and molecular pathology · 2013Article
- SAMe treatment prevents the ethanol-induced epigenetic alterations of genes in the Toll-like receptor pathway.Experimental and molecular pathology · 2013Article
- Alcoholic liver disease - Hepatocellular carcinoma transformation.Journal of gastrointestinal oncology · 2012Article
- Understanding Alcoholism Through microRNA Signatures in Brains of Human Alcoholics.Frontiers in genetics · 2012Article
- The role of innate immunity in the pathogenesis of preneoplasia in drug-induced chronic hepatitis based on a mouse model.Experimental and molecular pathology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Toll-like receptors (TLR) play a role in mediating the proinflammatory response, fibrogenesis and carcinogenesis in chronic liver diseases such as alcoholic liver disease, non-alcoholic liver disease, hepatitis C and hepatocellular carcinoma. This is true in experimental models of these diseases. For this reason, we investigated the TLR proinflammatory response in the chronic intragastric tube feeding rat model of alcohol liver disease. The methyl donor S-adenosylmethionine was also fed to prevent the gene expression changes induced by ethanol. Ethanol feeding tended to increase the up regulation of the gene expression of TLR2 and TLR4. SAMe feeding prevented this. TLR4 and MyD88 protein levels were significantly increased by ethanol and this was prevented by SAMe. This is the first report where ethanol feeding induced TLR2 and SAMe prevented the induction by ethanol. CD34, FOS, interferon responsive factor 1 (IRF-1), Jun, TLR 1,2,3,4,6 and 7 and Traf-6 were found to be up regulated as seen by microarray analysis where rats were sacrificed at high blood alcohol levels compared to pair fed controls. Il-6, IL-10 and IFNγ were also up regulated by high blood levels of ethanol. The gene expression of CD14, MyD88 and TNFR1SF1 were not up regulated by ethanol but were down regulated by SAMe. The gene expression of IL-1R1 and IRF1 tended to be up regulated by ethanol and this was prevented by feeding SAMe. The results suggest that SAMe, fed chronically prevents the activation of TLR pathways caused by ethanol. In this way the proinflammatory response, fibrogenesis, cirrhosis and hepatocellular carcinoma formation due to alcohol liver disease could be prevented by SAMe.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.