Down-regulation of NF-κB signalling by polyphenolic compounds prevents endotoxin-induced liver injury in a rat model

التفاصيل البيبلوغرافية
العنوان: Down-regulation of NF-κB signalling by polyphenolic compounds prevents endotoxin-induced liver injury in a rat model
المؤلفون: Jaideep S. Toor, Praveen Rishi, Sushma Bharrhan, Sunil K. Arora, Kanwaljit Chopra
المصدر: Innate immunity. 18(1)
سنة النشر: 2011
مصطلحات موضوعية: Immunology, Nitric Oxide Synthase Type II, Context (language use), Pharmacology, medicine.disease_cause, Nitric Oxide, Microbiology, Antioxidants, Catechin, Nitric oxide, chemistry.chemical_compound, Sepsis, medicine, Animals, Humans, Rats, Wistar, Molecular Biology, Liver injury, chemistry.chemical_classification, Reactive oxygen species, biology, Chemistry, Tumor Necrosis Factor-alpha, Liver Diseases, NF-kappa B, Polyphenols, Cell Biology, medicine.disease, Rats, Nitric oxide synthase, Endotoxins, Disease Models, Animal, Oxidative Stress, Infectious Diseases, NG-Nitroarginine Methyl Ester, Biochemistry, biology.protein, Female, Quercetin, Oxidative stress, Signal Transduction
الوصف: Activation of NF-κB has been reported to play a key role in causing endotoxin-induced hepatic damage through enhanced production of reactive oxygen species and pro-inflammatory mediators. In this context, the potential of polyphenolic phytochemicals in preventing endotoxin-induced liver damage remains unclear. Here, we demonstrate that catechin and quercetin have the potential to down-regulate the initial signalling molecule NF-κB which may further inhibit the downstream cascade including TNF-α and NO. These results were confirmed using N-nitro-L-arginine methyl ester (L-NAME), the inhibitor of inducible nitric oxide synthase (iNOS) along with the biochemical and histological alterations occurring in the presence and absence of supplementation with both the polyphenols. However, catechin was found to be more effective than quercetin against endotoxin-induced liver injury. These findings suggest that these polyphenols may form a pharmacological basis for designing a therapeutic agent against endotoxin-mediated oxidative damage.
تدمد: 1753-4267
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::261629ddc8142f3a7d6564c6193fccfc
https://pubmed.ncbi.nlm.nih.gov/21239456
Rights: OPEN
رقم الانضمام: edsair.doi.dedup.....261629ddc8142f3a7d6564c6193fccfc
قاعدة البيانات: OpenAIRE