The differential NF-kB modulation by S-adenosyl-L-methionine, N-acetylcysteine and quercetin on the promotion stage of chemical hepatocarcinogenesis
| Autor: | Olga Beltrán-Ramírez, Sandra Rosas, Samia Fattel-Fazenda, Rebeca García-Román, Jaime Arellanes-Robledo, Saúl Villa-Treviño, Daniel Salazar-González |
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| Rok vydání: | 2008 |
| Předmět: |
Male
S-Adenosylmethionine IκB kinase Pharmacology medicine.disease_cause Biochemistry Antioxidants Lipid peroxidation Acetylcysteine chemistry.chemical_compound Biomarkers Tumor medicine Animals Liver Neoplasms NF-kappa B NF-κB General Medicine Glutathione Rats Inbred F344 Rats Oxidative Stress Gene Expression Regulation chemistry Phosphorylation Quercetin Lipid Peroxidation Oxidative stress Signal Transduction medicine.drug |
| Zdroj: | Free Radical Research. 42:331-343 |
| ISSN: | 1029-2470 1071-5762 |
| DOI: | 10.1080/10715760802005169 |
| Popis: | S-adenosylmethionine (SAM), N-acetylcysteine (NAC) and quercetin exhibit a chemoprotective effect. Likely this effect is mediated by counteracting, oxidative stress and NF-kB activation. To test this hypothesis F344 rats were subjected to hepatocarcinogenesis with or without antioxidants. NAC decreased foci in number and area, SAM and quercetin decreased area. Lipid-peroxidation was decreased by antioxidants, but only SAM increased glutathione. SAM, in its regulation from IKK downwards, abolished the NF-kB activation. NAC decreased IKK and IkB-a phosphorylation, and Rel-A/p65 and NF-kB binding, though the last two were affected with less intensity compared to the NF-kB inhibitor. Quercetin decreased Rel-A/p65, without modifying upstream signalling. Although all antioxidants inhibited oxidative stress as shown by reduction of lipid peroxidation, not all exerted the same effect on NF-kB signalling pathway and only SAM increased GSH. The mechanisms exerted by SAM in the reduction of foci makes this compound a potential liver cancer therapeutic agent. |
| Databáze: | OpenAIRE |
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