| Green tea attenuates angiotensin II-induced cardiac hypertrophy in rats by modulating reactive oxygen species production and the Src/epidermal growth factor receptor/Akt signaling pathway. | |
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MedLine Citation:
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PMID: 18716156 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We previously documented a clear-cut antihypertensive effect of green teat extract (GTE), which was associated with correction of endothelial dysfunction and prevention of left ventricular hypertrophy in an angiotensin II (Ang II)-dependent model of hypertension, but the molecular mechanisms remain to be defined. As several effects of Ang II involve production of reactive oxygen species (ROS) and activation of 2nd messengers, such as mitogen-activated protein kinase (MAPK) and Akt, we investigated the effect of GTE on these signal transduction pathways in Ang II-treated rats. Rats were treated for 2 wk with Ang II infusion (700 mug.kg(-1).d(-1); n = 6, via osmotic minipumps), Ang II plus GTE (6 g/L) dissolved in the drinking water; n = 6), or vehicle (n = 6) to serve as controls. Blood pressure was monitored by telemetry throughout the study. The activation and expression of NAD(P)H oxidase subunits, protein kinase C isoforms, Src, epidermal growth factor receptor (EGFR), Akt, and MAPK were determined in the heart in vitro through immunoprecipitation and western blot analysis with specific antibodies. NAD(P)H oxidase enzymatic activity was measured by cytochrome c reduction assay. GTE blunted Ang II-induced blood pressure increase and cardiac hypertrophy. In Ang II-treated rats, GTE decreased the expression of the NAD(P)H oxidase subunit gp91(phox) and the translocation of Rac-1, as well as NAD(P)H oxidase enzymatic activity. Furthermore, it specifically reduced Ang II-induced Src, EGFR, and Akt phosphorylation. These results show that GTE blunts Ang II-induced cardiac hypertrophy specifically by regulating ROS production and the Src/EGFR/Akt signaling pathway activated by Ang II. |
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Authors:
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Italia Papparella; Giulio Ceolotto; Domenico Montemurro; Michele Antonello; Spiridione Garbisa; Gianpaolo Rossi; Andrea Semplicini |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of nutrition Volume: 138 ISSN: 1541-6100 ISO Abbreviation: J. Nutr. Publication Date: 2008 Sep |
Date Detail:
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Created Date: 2008-08-21 Completed Date: 2008-09-16 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0404243 Medline TA: J Nutr Country: United States |
Other Details:
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Languages: eng Pagination: 1596-601 Citation Subset: IM |
Affiliation:
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Department of Clinical and Experimental Medicine and Experimental Biomedical Sciences, University of Padova, 35128 Padova, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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toxicity Animals Cardiomegaly / chemically induced, drug therapy*, metabolism Enzyme Activation Isoenzymes Male Mitogen-Activated Protein Kinases / genetics, metabolism NADPH Oxidase / metabolism Oncogene Protein v-akt / genetics, metabolism* Protein Kinase C / chemistry, genetics, metabolism Protein Subunits Rats Rats, Sprague-Dawley Reactive Oxygen Species / metabolism* Receptor, Epidermal Growth Factor / metabolism* Signal Transduction Tea* src-Family Kinases / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Isoenzymes; 0/Protein Subunits; 0/Reactive Oxygen Species; 0/Tea; 11128-99-7/Angiotensin II; EC 1.6.3.1/NADPH Oxidase; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 2.7.10.2/src-Family Kinases; EC 2.7.11.1/Oncogene Protein v-akt; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.24/Mitogen-Activated Protein Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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