l-Carnitine ameliorates the oxidative stress response to angiotensin II by modulating NADPH oxidase through a reduction in protein kinase c activity and NF-κB translocation to the nucleus
Autor: | Sonia Zambrano, Ana Fortuño, Francisco M. González-Roncero, José L. Miguel-Carrasco, Alfonso Mate, Carmen Vázquez, Elisa Revilla, María V. Ruiz-Armenta, Antonio J. Blanca |
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Rok vydání: | 2015 |
Předmět: |
0301 basic medicine
medicine.medical_specialty p38 mitogen-activated protein kinases 030204 cardiovascular system & hematology Pharmacology Analytical Chemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine Carnitine medicine Animals Protein kinase B Protein kinase C Protein Kinase C NADPH oxidase biology Superoxide Nitrotyrosine Angiotensin II NF-kappa B NADPH Oxidases NF-κB General Medicine Oxidative Stress 030104 developmental biology Endocrinology chemistry Hypertension biology.protein Food Science |
Zdroj: | Food chemistry. 228 |
ISSN: | 1873-7072 |
Popis: | l-Carnitine (LC) exerts beneficial effects in arterial hypertension due, in part, to its antioxidant capacity. We investigated the signalling pathways involved in the effect of LC on angiotensin II (Ang II)-induced NADPH oxidase activation in NRK-52E cells. Ang II increased the generation of superoxide anion from NADPH oxidase, as well as the amount of hydrogen peroxide and nitrotyrosine. Co-incubation with LC managed to prevent these alterations and also reverted the changes in NADPH oxidase expression triggered by Ang II. Cell signalling studies evidenced that LC did not modify Ang II-induced phosphorylation of Akt, p38 MAPK or ERK1/2. On the other hand, a significant decrease in PKC activity, and inhibition of nuclear factor kappa B (NF-kB) translocation, were attributable to LC incubation. In conclusion, LC counteracts the pro-oxidative response to Ang II by modulating NADPH oxidase enzyme via reducing the activity of PKC and the translocation of NF-kB to the nucleus. |
Databáze: | OpenAIRE |
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