旋覆花中化学成分及其活性研究

综合运用硅胶柱色谱、凝胶柱色谱、制备HPLC色谱分离方法分离纯化旋覆花中的化学成分，采用NMR和质谱等有机波谱学方法鉴定各单体化合物的结构，进一步测试各化合物的抗炎活性。从旋覆花乙酸乙酯提取物中分离得到15个化合物，鉴定为二氢芥子醇（1），（3S，5R，6S，7E）-5，6-epoxy-3-hydroxy-7-megastigmen-9-one（2），（6R，7E）-9-hydroxy-4，7-megastigmadien-3-one（3），阿里二醇（4），蒲公英醇乙酸酯（5），8，9，10-三羟基百里香酚（6），花旗松素（7），木犀草素（8），泽兰黄酮（9），泽兰黄醇素（10），菠叶素（11），槲皮素（12），对羟基桂皮酸（13），咖啡酸（14），咖啡酸乙酯（15）。化合物 1，2，7，13，15 为首次从该属植物中分离得到，化合物 3，4，9~11，14 为首次从该种植物中分离得到。抗炎活性测定结果表明，化合物 3，6~12，14 具有明确的抑制c-Kit Ligand（KL） 诱导的肥大细胞白三烯C₄ （LTC₄） 生成和脱颗粒的作用，而且化合物 8和12 具有较强的抑制脂多糖（LPS）诱导的巨噬细胞RAW264.7细胞一氧化氮（NO） 释放作用。首次报道了黄酮类化合物 7，9~11 对LTC₄和肥大细胞脱颗粒具有较强的抑制作用。

Anti-inflammatory constituents from Inula japonica

Chemical constituents of Inula japonica were isolated and purifiedby repeated column chromatographies, over silica gel, and Toyopearl HW-40, and preparative HPLC. On the basis of spectral data analysis, including NMR and MS data, the structures of the isolates were elucidated and their anti-inflammatory activities were assayed. Fifteen compounds were isolated from the ethyl acetate extract of I.japonica, and their structures were elucidated as dihydrosyringenin(1),(3S,5R,6S,7E)-5,6-epoxy-3-hydroxy-7-megastigmen-9-one(2),(6R,7E)-9-hydroxy-4,7-megastigmadien-3-one(3), arnidiol(4), taraxasterol acetate(5), 8,9,10-trihydroxythymol(6), taxifolin(7), luteolin(8), napetin(9), eupatin(10), spinacetin(11), quercetin(12), p-hydroxycinnamic acid(13), caffeic acid(14), and caffeoyl acetate(15). Compounds 1, 2, 7, 13 and 15 were isolated from the genus Inula for the first time, and compounds 3, 4, 9-11 and 14 were isolated from this plant for the first time. The anti-inflammatory activity result showed that compounds 3, 6-12 and 14 exhibited inhibition effect against leukotriene C₄ (LTC₄) synthesis and degranulation definitely in c-Kit Ligand(KL) induced mast cells, and compound 8 and 12 also had the suppression effect against lipopolysacharide(LPS) induced nitric oxide(NO) activity in RAW264.7 macrophages. It is firstly reported that compounds 7 and 9-11 possessed potent inhibition activities against LTC₄ generation and degranulation in mast cells.