Genistein Inhibits Expressions of NADPH Oxidase p22phox and Angiotensin II Type 1 Receptor in Aortic Endothelial Cells from Stroke-Prone Spontaneously Hypertensive Rats
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- XU Jin-Wen
- Frontier Health Science, School of Human Environmental Science, Mukogawa Women’s University Research Center for Life-Style Related Diseases, Mukogawa Women’s University
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- IKEDA Katsumi
- Frontier Health Science, School of Human Environmental Science, Mukogawa Women’s University Research Center for Life-Style Related Diseases, Mukogawa Women’s University
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- YAMORI Yukio
- WHO Collaborating Center for Research on Primary Prevention of Cardiovascular Diseases
書誌事項
- タイトル別名
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- <B>Genistein Inhibits Expressions of NADPH Oxidase p22phox and Angiotensin II Type 1 Receptor in Aortic Endothelial Cells from Stroke-Prone Spontaneously Hypertensive Rats</B>
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抄録
Phytoestrogens are considered to be natural selective estrogen receptor modulators exerting antioxidant activity and improving vascular function. However, the mechanisms responsible for their antioxidative effects remain largely unknown. This study tested the hypothesis that genistein may provide significant endothelial protection by antioxidative effects through attenuating NADPH oxidase expression and activity. The results showed that genistein suppressed the expressions of the p22phox NADPH oxidase subunit and angiotensin II (Ang II) type 1 (AT1) receptor in a concentration- and time-dependent manner in aortic endothelial cells from stroke-prone spontaneously hypertensive rats examined by Western blot analysis. Treatment with genistein also remarkably reduced the Ang II-induced superoxide by the reduction of nitroblue tetrazolium, inhibited nitrotyrosine formation, and attenuated endothelin-1 production by ELISA via the stimulation of Ang II. However, when cells were pretreated with ICI-182780, an estrogen-receptor antagonist, at a concentration of 50 μmol/l for 30 min and then co-incubated with ICI-182780 and genistein for 24 h, the inhibitory effect of genistein was not blocked. In contrast, the inhibitory effect of genistein treatment was partially reversed by 30-min pretreatment of endothelial cells with GW9662, a peroxisome proliferator-activated receptor γ (PPARγ) antagonist. Genistein thus appears to act as an antioxidant at the transcription level by the downregulation of p22phox and AT1 receptor expression. Our data also showed that the PPARγ pathway was involved, at least in part, in the inhibitory effect of genistein on the expression of p22phox and AT1 receptors. The endothelial-protective effects of phytoestrogen may contribute to improvement of cardiovascular functions. (Hypertens Res 2004; 27: 675-683)
収録刊行物
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- Hypertension Research
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Hypertension Research 27 (9), 675-683, 2004
日本高血圧学会
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詳細情報
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- CRID
- 1390001204719477504
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- NII論文ID
- 130004437187
- 10014047684
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- NII書誌ID
- AA10847079
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- COI
- 1:CAS:528:DC%2BD2MXnt1antw%3D%3D
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- ISSN
- 13484214
- 09169636
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- PubMed
- 15750262
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可