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ANTIMUTAGENIC ACTIVITY OF FALCARINDIOL FROM PEUCEDANUM PRAERUPTORUM

机译:白头翁中地卡因的抗拒活性

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A methanol extract from Peucedanum praeruptorum showed a suppressive effect on umu gene expression of the SOS response in Salmonella typhimurium TA1535/pSK1002 against the mutagen 2-(2-furyl)-3-(5-nitro-2-furyl)acrylamide (furylfuramide). The methanol extract from P. praeruptorum was re-extracted with hexane, dichloromethane, n-butanol, and water, respectively. A suppressive compound in the hexane extract fraction was isolated by SiO2 column chromatography and identified as falcarindiol by EI-MS, IR, and H-1 and C-13 NMR spectroscopy. Falcarindiol exhibited an inhibition of the SOS-inducing activity of furylfuramide in the umu test. Gene expression was suppressed 75% at less than 0.15 mu mol/mL, and the ID50 value was 0.10 mu mol/mL. The diacetate compound of falcarindiol did not show any suppressive effect on the SOS induction of furylfuramide. Falcarindiol was also assayed with the mutagen 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1), which requires liver-metabolizing enzymes, and showed a suppressive effect similar to that with furylfuramide. The falcarindiol ID50 value versus Trp-P-1 was 0.096 mu mol/mL. The antimutagenic activities of falcarindiol and falcarindiol diacetate against furylfuramide and Trp-P-1 were tested by an Ames test using S. typhimurium TA100, which indicated that falcarindiol suppressed the mutagenicity of furylfuramide and Trp-P-1 and falcarindiol diacetate suppressed the mutagenicity of Trp-P-1.
机译:百日草甲醇提取物对鼠伤寒沙门氏菌TA1535 / pSK1002中针对诱变剂2-(2-呋喃基)-3-(5-硝基-2-呋喃基)丙烯酰胺(呋喃基呋喃酰胺)的SOS响应的umu基因表达具有抑制作用。 。分别用己烷,二氯甲烷,正丁醇和水分别萃取自P. praeruptorum提取的甲醇。通过SiO2柱色谱法分离己烷萃取液馏分中的抑制性化合物,并通过EI-MS,IR和H-1和C-13 NMR光谱将其鉴定为法卡林二醇。在umu试验中,法卡林二醇对呋喃基呋喃酰胺的SOS诱导活性具有抑制作用。在小于0.15μmol/ mL下,基因表达被抑制了75%,ID50值为0.10μmol/ mL。法卡林二醇的二乙酸酯化合物对呋喃呋喃酰胺的SOS诱导没有抑制作用。还使用需要肝脏代谢酶的诱变剂3-氨基-1,4-二甲基-5H-吡啶并[4,3-b]吲哚(Trp-P-1)测定了法卡林二醇。与呋喃呋喃酰胺。相对于Trp-P-1而言,心果二醇ID50值为0.096μmol/ mL。使用鼠伤寒沙门氏菌TA100进行Ames试验,检测了草丁二醇和草丁二醇二乙酸酯对呋喃基呋喃酰胺和Trp-P-1的抗诱变活性,这表明,草丁二醇抑制了呋喃呋喃酰胺和Trp-P-1的致突变性,而草丁二醇二乙酸酯则抑制了呋喃呋喃酰胺和Trp-P-1的致突变性。 Trp-P-1。

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