Green tea modulation of inducible nitric oxide synthase in hypoxic/reoxygenated cardiomyocytes

Hypoxia/reoxygenation (H/R) is one of the causes of the increased expression of inducible nitric oxide synthase (iNOS) in cardiomyocytes. Since an aberrant NOS induction has detrimental consequences, we evaluated the effect of a green tea extract (GTE) on the NOS induction and activity in H/R-cardio...

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Bibliographic Details
Published in:Biochimie 2005-05, Vol.87 (5), p.457-460
Main Authors: Agnetti, G., Bordoni, A., Angeloni, C., Leoncini, E., Guarnieri, C., Caldarera, C.M., Biagi, P.L., Hrelia, S.
Format: Article
Language:English
Subjects:
Animals
Cardiomyocytes
Catechins
Cell Hypoxia
Cells, Cultured
Dietary Supplements
Gene Expression Regulation, Enzymologic
Green tea
Hypoxia/reoxygenation
Myocytes, Cardiac - drug effects
Myocytes, Cardiac - enzymology
Nitric oxide synthase
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Oxygen - metabolism
Rats
Rats, Wistar
Tea
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Summary:Hypoxia/reoxygenation (H/R) is one of the causes of the increased expression of inducible nitric oxide synthase (iNOS) in cardiomyocytes. Since an aberrant NOS induction has detrimental consequences, we evaluated the effect of a green tea extract (GTE) on the NOS induction and activity in H/R-cardiomyocytes to define a nutritional strategy. Cultured rat cardiomyocytes were exposed to H/R in the presence of two concentrations of a green tea extract (GTE), which is reported to inhibit NOS expression and activity in different cells. In cultured cardiomyocytes two NOS isoforms were constitutively expressed, but only iNOS was induced by H/R. GTE supplementation at the lowest concentration, comparable to that in human plasma after dietary consumption, was ineffective, while the highest, comparable to that achievable by dietary supplements, counteracted the effect of H/R on iNOS induction and activity. It is necessary to verify in humans the relationship between the modulation of NO production and green tea dietary consumption.
ISSN:0300-9084
1638-6183
DOI:10.1016/j.biochi.2005.01.004