期刊名称：Journal of Clinical Biochemistry and Nutrition
印刷版ISSN：0912-0009
电子版ISSN：1880-5086
出版年度：2011
卷号：48
期号：1
页码：85-90
DOI：10.3164/jcbn.11-004FR
出版社：The Society for Free Radical Research Japan
摘要：Gallic acid is widely distributed in plants, fruits and foods with a range of biological activities. In the present study the possible mechanisms of gallic acid anticancer properties were explored in A549, a human lung adenocarcinoma cell line. Our study shows that it inhibited the A549 cell growth and decreased cell viability monitored at 24 h. It also inhibited cell proliferation in dose- and time-dependent manner as measured by 3-[4,5-methylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide assay at 24 and 48 h. Morphological examination of the cells after gallic acid treatment showed the typical feature of cell death such as cell shrinkage and rounding up of the cells. Clonogenic assay indicated that gallic acid treatments inhibited the colony formation. DNA fragmentation assay indicated the disappearance of the genomic DNA in dose-dependent manner. To find out possible mechanisms, mitochondrial potential and intracellular reactive oxygen species were measured. It was observed that gallic acid treatment decreased mitochondrial membrane potential and increased intracellular reactive oxygen species. Further caspases activity was measured and it was found that gallic acid activated the caspase-3 but not caspase-8 indicating the involvement of intrinsic pathway of cell apoptosis.
关键词：apoptosis;adenocarcinoma;DNA damage;reactive oxygen species
