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Anticancer property of gallic acid in A549, a human lung adenocarcinoma cell line, and possible mechanisms

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...

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Detalles Bibliográficos
Autores principales: Maurya, Dharmendra K., Nandakumar, Nivedita, Devasagayam, Thomas Paul Asir
Formato: Texto
Lenguaje:English
Publicado: the Society for Free Radical Research Japan 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022071/
https://www.ncbi.nlm.nih.gov/pubmed/21297918
http://dx.doi.org/10.3164/jcbn.11-004FR
Descripción
Sumario: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.