Wei Bai-Luh, Weng Jing-Ru, Chiu Pao-Hui, Hung Chi-Feng, Wang Jih-Pyang, Lin Chun-Nan
Institute of Life Science, National Taitung University, Taitung, Taiwan 950, Republic of China.
J Agric Food Chem. 2005 May 18;53(10):3867-71. doi: 10.1021/jf047873n.
The antiinflammatory activities of the isolated flavonoids, including cycloartomunin (1), cyclomorusin (2), dihydrocycloartomunin (3), dihydroisocycloartomunin (4), cudraflavone A (5), cyclocommunin (6), and artomunoxanthone (7), and cycloheterohyllin (8), artonins A (9) and B (10), artocarpanone (11), artocarpanone A (12), and heteroflavanones A (13), B (14), and C (15) from Artocarpus communis and A. heterophyllus, were assessed in vitro by determining their inhibitory effects on the chemical mediators released from mast cells, neutrophils, and macrophages. Compound 4 significantly inhibited the release of beta-glucuronidase and histamine from rat peritoneal mast cells stimulated with P-methoxy-N-methylphenethylamine (compound 48/80). Compound 11 significantly inhibited the release of lysozyme from rat neutrophils stimulated with formyl-Met-Leu-Phe (fMLP). Compounds 8, 10, and 11 significantly inhibited superoxide anion formation in fMLP-stimulated rat neutrophils while compounds 2, 3, 5, and 6 evoked the stimulation of superoxide anion generation. Compound 11 exhibited significant inhibitory effect on NO production and iNOS protein expression in RAW 264.7 cells. The potent inhibitory effect of compound 11 on NO production in lipopolysaccharide (LPS)-activated macrophages, probably through the suppression of iNOS protein expression.
从面包树和木菠萝中分离得到的黄酮类化合物,包括环木菠萝素(1)、环桑皮素(2)、二氢环木菠萝素(3)、二氢异环木菠萝素(4)、柘树黄酮A(5)、环桑皮亭(6)、面包树氧杂蒽酮(7)、环异叶山小橘素(8)、波罗蜜宁A(9)和B(10)、面包木酮(11)、面包木酮A(12)以及异黄酮A(13)、B(14)和C(15)的抗炎活性,通过测定它们对肥大细胞、中性粒细胞和巨噬细胞释放的化学介质的抑制作用在体外进行了评估。化合物4显著抑制了用对甲氧基-N-甲基苯乙胺(化合物48/80)刺激的大鼠腹膜肥大细胞中β-葡萄糖醛酸酶和组胺的释放。化合物11显著抑制了用甲酰甲硫氨酰亮氨酰苯丙氨酸(fMLP)刺激的大鼠中性粒细胞中溶菌酶的释放。化合物8、10和11显著抑制了fMLP刺激的大鼠中性粒细胞中超氧阴离子的形成,而化合物2、3、5和6则诱导了超氧阴离子生成的刺激。化合物11对RAW 264.7细胞中一氧化氮(NO)的产生和诱导型一氧化氮合酶(iNOS)蛋白表达具有显著的抑制作用。化合物11对脂多糖(LPS)激活的巨噬细胞中NO产生的强效抑制作用,可能是通过抑制iNOS蛋白表达实现的。