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頁籤選單縮合
題名 | Receptor-Dependent and Genomic-Independent Actions of Estrogen in Vascular Protection=雌激素引發受體依賴性但非基因體依賴性之血管保護作用 |
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作者姓名(中文) | 樓迎統; | 書刊名 | 長庚醫學 |
卷期 | 25:10 2002.10[民91.10] |
頁次 | 頁636-644 |
分類號 | 418.276 |
關鍵詞 | 雌激素; 一氧化氮; 雌激素受體; 內皮一氧化氮合成; 磷脂激酶; 血管功能; Estrogen; Nitric oxide; Estrogen receptor; Endothelial nitric oxide synthase; Phosphatidylinositol 3-kinase; Vascular functions; |
語文 | 英文(English) |
中文摘要 | 雌激素可以經由受體媒介,但係非基因體依賴性的快速作用引起很多興趣。雖然雌激素受體本質仍不清楚,快速作用可以被受體拮抗劑抑制,也可以被不能通過細胞膜之雌激素型劑模倣。因為內皮膜產生一氧化氮(NO)是重要調控心血管的機制,雌激素保護心血管的機轉中也以增加NO生產為鋹要管道。在活體或體外實驗中,不少證據顯示雌素活化內皮NO合成?(eNOS)刺激NO產生。近來研究更發現雌激素經快速活化磷脂激?(PI3-K)訊息傳遞系統,刺激內皮NO合成。這些觀察代表在血管細胞中雌激素快速且經受體媒介(但非轉錄依賴性)的作用可能參與保護心血管。本文回顧最近的相關證據並討論血管雌激素受體之生理意義。 |
英文摘要 | Functional evidence for a rapid, receptor-dependent and genomic-independent action of estrogen in vascular cells continues to accumulate. Although the nature of the receptor is nto yet clear, some of the hormone-induced effects can be blocked by known estrogen antagonists (e.g., ICI 182, 780) and can be mimicked by membrane-impermeable forms of estrogen. Because the endothelial output of nitric oxide (NO) is a major regulator of several cardiovascular functions, regulation of NO production has received a lot of attention as a potential mechanism for the cardiovascular protection offered by estrogen. There is ample eviddnce that estrogen can stimulate NO production and activate endothelial NO synthase (eNOS) both in vitro and in vivo. Recent investigations have shown that estrogen’s rapid stimulatory action on eNOS is mediated by the activation of phosphatidylinositol 3-kinase (PI3-K) and protein kinase B (PKB)/Akt pathway among other signaling systems. Although these effects are estrogen receptor-dependent, they are rapid (on the order of a few minutes) and transcription-independent and thus represent genomic-independent but receptor-mediated effects of a steroid operating in vascular cells. In this review, recent evidence for such mechanisms is summarized, and the role of estrogen receptors in vivo is also briefly discussed. |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。