蔥青水萃取物抗發炎之機制探討

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標題:	蔥青水萃取物抗發炎之機制探討 Anti-inflammatory effects of aqueous extract from Welsh onion green leaves
作者:	林協信 Shie-Shin Lin
貢獻者:	范晉嘉王柏森嘉南藥理科技大學：生物科技研究所
關鍵字:	巨噬細胞蔥青水萃取物脂多醣極低密度脂蛋白一氧化氮環氧化酶一氧化氮合成酶 COX-2 iNOS Very low density lipoprotein(VLDL) Lipopolysaccharide (LPS) Welsh onion green leaves extract (WOE)
日期:	2003
上傳時間:	2008-10-08 15:45:41 (UTC+8)
摘要:	目前研究皆指出，在粥狀動脈硬化形成過程中，發炎反應扮演著重要的角色，因為在發炎過程中，誘導型一氧化氮合成酶(iNOS)和環氧化酶(COX-2)在極短時間內會產生過量的一氧化氮(Nitric oxide; NO)與前列腺素(Prostaglandin H2; PGH2)，進而啟動粥狀動脈硬化的形成。在我們的實驗中發現，蔥青水萃取物(WOE)具有捕捉自由基(ABTS+)的能力，並可抑制低密度脂蛋白(LDL)及去氧五碳醣(Deoxyribose; DR)的氧化分解。此外，不同濃度之青蔥水萃取物對於由脂多醣或極低密度脂蛋白刺激之巨噬細胞(RAW 264.7)活化產生之亞硝酸鹽(Nitrite)有抑制作用，且無明顯之細胞毒性產生。其作用機轉以西方墨點法分析蛋白表現，蔥青水萃取物抑制脂多醣及極低密度脂蛋白所誘發的iNOS、COX-2及CD36蛋白表現。以RT-PCR方法分析mRNA，發現青蔥水萃取物亦可抑制脂多醣及極低密度脂蛋白增加iNOS及CD36 mRNA量。此外，蔥青水萃取液和N-Methyl-L-arginine acetate(NOS 抑制劑)、aminoquanidine(NOS 抑制劑)、quercetin(酪氨酸激酶抑制劑)、PDTC (NF-κB inhibitor)、TPCK (Serine protease inhibitor)等不同之細胞內訊息傳導抑制劑共同處理時，皆有加強其抑制作用。綜合這些實驗結果，我們推論青蔥水萃取液可以抑制發炎反應中，一氧化氮合成酶和環氧化酶此二種酵素之表現，進而對於粥狀動脈硬化的形成，可能有預防保健的功效。 Many studies have reported that inflammation play a important role in atherosclerosis development. Through inflammation process, in macrophages, production of excess nitric oxide and prostaglandin H2 in short time by inducible nitric oxide synthase (iNOS) and cyclooxygenase- 2 (COX-2) make initial formation of atherosclerosis. In our present study, we find Welsh onion green leaves extract (WOE) can scavenge free radical (ABTS+), and inhibit low-density lipoprotein (LDL) and deoxyribose (DR) oxidized degradation. In addition dose-dependent of WOE can inhibit nitrite production in lipopolysaccharide (LPS) or very-low density lipoprotein (VLDL) stimulated macrophage RAW264.7 cells, and without obviously cytotoxic effect. WOE also can suppress LPS and VLDL induced iNOS, COX-2 and CD36 protein measured by Western blot. A similar pattern was observed in WOE inhibit LPS and VLDL to increase iNOS and CD36 mRNA expression measured by RT-PCR. Moreover, co-treatment WOE with NG-methyl-L-arginine acetate (a NOS inhibitor), Aminoguanidine (a NOS inhibitory), Quercetin (a tyrosine kinase inhibitor), Pentoxifylline (a phosphodiesterase inhibitor), Pyrrolidine dithiocarbamate (a NFkB inhibitor), TPCK (a serine protease inhibitor) also can promote the inhibition extent than WOE treatment alone. These results suggest that inhibition of iNOS, COX-2 and CD36 expression by WOE may be responsible for WOE’s healthful effect in anti-atherosclerosis.
關聯:	校內校外均不公開
显示于类别:	[生物科技系(所)] 博碩士論文

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