Taipei Medical University Institutional Repository:Item 987654321/5189
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    题名: 3-Methylquercetin對離體天竺鼠氣管的鬆弛作用
    Relaxant Effect of 3-Methylquercetin in Isolated guinea Pig Trachea
    作者: 王漢琅
    Wang, Han-Lang
    贡献者: 醫學研究所
    关键词: 天竺鼠
    鬆弛作用
    日期: 1994
    上传时间: 2009-09-11 15:25:38 (UTC+8)
    摘要: 3-Methylquercetin(3-MQ)可使離體天竺鼠氣管產生鬆弛作用，它對histamine(30μM、carbachol(0.2 μM)及isotonic KCI(17.5mM)預先收縮的IC50分別為13.98±2.54(n=7)、14.56±0.92(n=6)及21.15±2.92(n=9)μM，彼此間無意義差，顯示無特殊選擇性。
    3-MQ(30μM)預處理20分鐘，對累加histamine引起的收縮呈非競爭性的抑制，求得的pD2'值為5.29±0.15(n=8)，有意義的大於鬆弛histamine(30μM)預縮的-logIC50，顯示對內鈣釋放的抑制較有選擇性。3-MQ(30μM)對高鉀(60mM)無鈣溶液，因外鈣增加而引起的收縮，能有意義的抑制，顯示它會抑制外鈣經由voltage dependent calcium cliannel (VDC)的流入。然而對histamine(30 μM)的預縮，它能夠使nifedipine(10μM)的最大鬆弛進一步鬆弛，顯示它除了可能抑制VDC外尚有其他鬆弛機轉。
    3-MQ的鬆弛作用無須仰賴上皮細胞，亦與β-受體活化或鉀通道開啟無關。它的鬆弛作用不被2',5'-dideoxyadenosine(10μM)、methylene blue(25μM)或oxyhemoglobin(10μM)所影響，顯示它的鬆弛作用並非活化 adenylate cyclase 或 guanylate cyclase而來。但它(30-100μM)類似protein kinase C (PKC)抑制劑staurosporine(0.003-1μM)能劑量依存性地抑制PKC活化劑phorbol 12-myristate 13-acetate(10μM)引起的氣管收縮，因此它對PKG可能也有抑制作用，而使氣管平滑肌鬆弛。因3-MQ(15μ M)也會使staurosporine(1μM) ;或nifedipine(10μM)及staurosporine(1μM)之共同存在下的最大鬆弛進一步鬆弛，因此不能排除它抑制PKC外，尚有其他鬆弛機轉。3-MQ(7.5及15μM)像3-isobutyl-1-methyl-xanthine(3及6μM)能使累積用量方式加入的forskolin或nitroprusside之對數劑量-反應曲線向左平行移 動，而且呈劑量依存性，顯示它也有可能會抑制phosphodiesterase (PDE)。
    3-MQ使氣管鬆弛的可能機轉包括抑制外鈣流入和內鈣釋放、抑制PKC及抑制PDE而來。
    3-Methylquercetm (3-MQ) had relaxant effects in guinea pig trachealis. Its IC50 was 13.98±2.54 (n=7), 14.56±0.92 (n=6) and 21.15 ± 2.92 (n=9) μM for the precontractions induced by histamine (30 μM), carbachol (0.2 μM) and isotonic KC1 (17.5 mM), respectively. There was no significant difference among them. It shows that 3-MQ has no special selectivity to these three contractile agents.
    Pretreatment of tracheahs with 3-MQ (30 μM) for 20 min non- competitively inhibited the contractions induced by cumulative histamine. Its calculated pD2' value was 5.29 ±0.15 (n=8). It is significantly greater than the -logIC50 for the precontraction induced by histamine (30 μM). It shows that 3-MQ selectively inhibits more on the calcium release from intracellular calcium stores. 3-MQ (30 μM) significantly inhibited the cumulative calcium-induced contractions in guinea pig trachealis, incubated in high potassium (60 mM) calcium-free medium. This suggests that 3-MQ may inhibit calcium influx through voltage dependent calcium channels (VDC). However, it produced further relaxation after nifedipine (10 μM)-induced maximal relaxation. This suggests that 3-MQ may have other relaxing mechanism in addition to its inhibiting VDC.
    The relaxant effect of 3-MQ was epithelium-independent, and was not correlated to β adrenoreceptor activation or potassium channel opening. Its relaxant effect was not affected by 2',5'- dideoxyadenosme (10μM), methylene blue (25 μM) or oxyhemoglobin (10 μM). The data suggest that the relaxant effect of 3-MQ may be not via activation of adenylate cyclase or guanylate cyclase. However, 3-MQ, similar to protein kinase C (pKC) inhibitor staurosporme (0.003-1 μM), dose-dependently inhibited the precontraction induced by phorbol 12-myristate 13- acetate (10 μM), an activator of PKC in guinea pig trachealis. Therefore the relaxant effect of 3-MQ may also be via inhibiting the PKC activity. However, 3-MQ (15 μM) produced further relaxation after the relaxant effect produced by either staurosporme (1 μM)- or nifedipine (10 μM) and staurosporine (1 μM). Therefore it may have additional relaxing mechanism. 3- MQ (7.5 and 15 μM), similar to 3-isobutyl-1-methyl-xanthine (3 and 6 μM), parallelly shifted leftward the log dose-response curves of forskolin and nitroprusside in a dose-dependent phasion. This shows that 3-MQ may also inhibit activity of phosphodiesterase (PDE).
    3-MQ may relax tracheali via inhibition of calcium influx, calcium release from intracellular calcium stores, PKC, and PDE.
    数据类型: thesis
    显示于类别:[醫學科學研究所] 博碩士論文

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