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目的:比较离舌橐吾Ligularia veitchiana(Hemsl.)Greenm的2种苯并呋喃衍生物5,6-二甲氧基-2-异丙基-苯并呋喃(5,6-dimethoxy-2-isopropenyl-benzofuran,化合物1),5-乙酰基-6-甲氧基-2-异丙基-苯并呋喃(5-acetyl-6-methoxy-2-isopropenyl-benzofuran,化合物2)对人肝癌细胞HepG2和正常肝细胞L02的毒性,并分析其可能机制。方法:用台盼蓝排染法检测化合物细胞毒性、用DCFH-DA荧光分光光度计法检测细胞活性氧含量、用钼酸铵比色法检测过氧化氢酶活性。结果:化合物1和2对L02的IC50分别为(171.2±3.3)mg·L-1和(79.0±4.1)mg·L-1,高于对HepG2的IC50(84.2±6.5)mg.L-1和(65.2±1.9)mg·L-1,表明肿瘤细胞比正常细胞对化合物更加敏感。用化合物1和2 IC50处理细胞48 h,测得HepG2细胞活性氧分别是对照组的1.6倍和3.2倍;L02细胞活性氧分别是对照组的1.2倍和1.8倍。化合物1和2处理后,HepG2细胞过氧化氢酶活力分别从对照组的(17.2±1.7)U·mg-1下降到(12.8±0.4)和(6.4±0.1)U·mg-1;L02细胞过氧化氢酶活力分别从对照组的(17.7±1.2)U·mg-1下降到(14.3±1.5)和(8.6±0.5)U·mg-1;HepG2过氧化氢酶活力降低幅度大于L02。结论:2个化合物对HepG2的毒性和活性氧的增幅均大于L02,同时HepG2过氧化氢酶活力降幅也大于L02。据此推测2个化合物细胞毒性与活性氧有关。
Objective: To compare the inhibitory effects of two benzofuran derivatives, 5,6-dimethoxy-2-isopropenyl (5-dimethoxy-2-isopropenyl) -benzofuran, compound 1), 5-acetyl-6-methoxy-2-isopropenyl-benzofuran (compound 2) on human hepatocellular carcinoma cells HepG2 And normal liver cells L02 toxicity, and analyze its possible mechanism. Methods: The cytotoxicity of compound was determined by trypan blue exclusion method. The content of reactive oxygen species (ROS) in cells was detected by DCFH-DA fluorescence spectrophotometer. The activity of catalase was assayed by ammonium molybdate colorimetry. Results: The IC50 of compounds 1 and 2 to L02 were (171.2 ± 3.3) mg · L-1 and (79.0 ± 4.1) mg · L-1, respectively, higher than that of HepG2 (84.2 ± 6.5) mg.L-1 And (65.2 ± 1.9) mg · L -1, respectively, indicating that tumor cells are more sensitive to the compounds than normal cells. The cells treated with IC50 of IC50 for 1 and 2 for 48 h showed that the active oxygen of HepG2 cells were 1.6 and 3.2 times that of the control group respectively. The reactive oxygen species of L02 cells were 1.2 times and 1.8 times that of the control group respectively. The activities of catalase in HepG2 cells decreased from (17.2 ± 1.7) U · mg-1 to (12.8 ± 0.4) and (6.4 ± 0.1) U · mg-1 in HepG2 cells after treatment with compounds 1 and 2. L02 cells The catalase activity decreased from (17.7 ± 1.2) U · mg-1 to (14.3 ± 1.5) and (8.6 ± 0.5) U · mg-1 in the control group, respectively; the decrease of HepG2 catalase activity was greater than L02. Conclusion: The toxicity of 2 compounds to HepG2 and the increase of reactive oxygen species are both greater than L02, and the decrease of HepG2 catalase activity is also greater than that of L02. It is speculated that the two compounds cytotoxicity and reactive oxygen species.