ArticleThe Kaohsiung journal of medical sciences2014
Protective effect of chitosan treatment against acetaminophen-induced hepatotoxicity.
Article in The Kaohsiung journal of medical sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 40 citations in OpenAlex.
- Protective Effects of Propolis and Chitosan Nanoparticles against Ibuprofen-Induced Hepatotoxicity in Albino Rats.Diseases (Basel, Switzerland) · 2024Article
- Morin encapsulated chitosan nanoparticles (MCNPs) ameliorate arsenic induced liver damage through improvement of the antioxidant system and prevention of apoptosis and inflammation in mice.Nanoscale advances · 2022Article
- The Use of Chitosan-Coated Nanovesicles in Repairing Alcohol-Induced Damage of Liver Cells in Mice.Medicina (Kaunas, Lithuania) · 2022Article
- Effect of betulinic acid administration on TLR-9/NF-κB /IL-18 levels in experimental liver injuryTurkish journal of medical sciences · 2021Article
- The Evaluation of Drug Delivery Nanocarrier Development and Pharmacological Briefing for Metabolic-Associated Fatty Liver Disease (MAFLD): An Update.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Novel Therapies for the Treatment of Drug-Induced Liver Injury: A Systematic Review.Frontiers in pharmacology · 2021Review
- Gold Nanoparticles Perturb Drug-Metabolizing Enzymes and Antioxidants in the Livers of Male Rats: Potential Impact on Drug Interactions.International journal of nanomedicine · 2020Article
- Therapeutic effect of chitosan on CCl4‑induced hepatic fibrosis in rats.Molecular medicine reports · 2018Article
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetaminophen (APAP) is the most commonly reported toxic ingestion in the world. Severe liver injury resulting from overdose or chronic use of APAP remains a significant clinical problem. In recent years, the mechanisms underlying liver injury caused by APAP have become much better understood. We have studied the protective effect of chitosan supplementation against APAP-induced hepatotoxicity with respect to changes in the levels of total and lipid-bound sialic acid in the serum and in the liver tissue and changes in the activity of diagnostic marker enzymes, lipid peroxidation, and ceruloplasmin oxidase enzyme in normal and experimental groups of rats. During the experimental period, chitosan (200 mg/kg body weight per day) was administered to APAP + chitosan-treated rats by oral gavage. Results showed that treatment with APAP induced a significant increase in the serum alanine aminotransferase and alkaline phosphatase activities, in total and lipid-bound sialic acids levels, and in the liver lipid peroxide content. The administration of chitosan significantly prevented APAP-induced alterations in the levels of diagnostic marker enzymes, total sialic acid, lipid-bound sialic acid, and malondialdehyde in the experimental groups of rats. Furthermore, chitosan administration increased the activity of ceruloplasmin oxidase. In conclusion, our results suggest that chitosan has a protective effect on APAP-induced hepatic injury in rats. The study sheds light on the therapeutic potential of chitosan in an APAP-induced hepatotoxicity model.
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