書誌事項
- タイトル別名
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- プラークナイ ケッカン シンセイ ニ オヨボス カテキン ノ エイキョウ バイヨウ ナイヒ サイボウ オ モチイタ ケントウ
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type:P(論文)
Blood vessel formation after birth (angiogenesis), occurs within ischemic lesion to salvage jeopardized hypoxic cells. It also occurs within atherosclerotic plaques in which inflammatory cells are releasing angiogenic factors. However, angiogenesis in atherosclerotic plaque increases the vulnerability of plaque and the incidence of symptomatic atherosclerotic diseases. Therefore, the inhibition of angiogenesis in plaque could prevent unstabilization of the plaque and the resulting ischemic disease. Vascular endothelial growth factor (VEGF) is one of key regulators of angiogenesis. Lysophosphatidylcholine (LysoPC) and sphingosine - 1 - phosphate (SIP), which are contained in low density lipoprotein (LDL) and oxidized LDL, are two major modifiers of VEGF action in atherosclerotic plaque. We applied these substances on cultured bovine vascular endothelial cells (BAEC) to mimic angiogenesis in atherosclerosis in vitro, and examined whether epigallocatechin - 3 - gallate (EGCG), the major green tea catechin, has inhibitory effects on plaque angiogenesis. The effects of catechins were tested in three models of angiogenesis, namely, migration, growth and tube formation of BAEC. EGCG inhibited angiogenesis in vitro in Boyden chamber assay for migration step, cell counting assay for growth step and matrigel assay for tube formation step at concentration ranging from 1 to 50μM. Therefore, EGCG could stabilize atherosclerotic plaques by inhibiting angiogenesis and prevent them from rupture.
収録刊行物
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- 神戸女学院大学論集 = KOBE COLLEGE STUDIES
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神戸女学院大学論集 = KOBE COLLEGE STUDIES 54 (1), 95-109, 2007-06-20
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詳細情報 詳細情報について
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- CRID
- 1390572174603727360
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- NII論文ID
- 110007043181
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- NII書誌ID
- AN00085725
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- ISSN
- 03891658
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- NDL書誌ID
- 8909900
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- IRDB
- NDL
- CiNii Articles