cytotoxicity of selected novel chalcone derivatives on human breast, lung and hepatic carcinoma cell lines

Authors

maryam nakhjavani department of pharmaco-toxicology, shahid beheshti university of medical sciences, tehran, iran. p.o.box 14155-6153

afshin zarghi department of medicinal chemistry, shahid beheshti university of medical sciences, tehran, iran. p.o.box 14155-6153

farshad h. shirazi department of pharmaco-toxicology, shahid beheshti university of medical sciences, tehran, iran. p.o.box 14155-6153 pharmaceutical sciences research center, shahid beheshti university of medical sciences, tehran, iran. p.o.box 14155-3817

abstract

cancer is considered as a challenging deathly disease and discovering or synthesis of new cytotoxic agents is a worldwide attempt. in this study, a group of recently synthesized chalcones, with the structure of 1,3-diarylprop-2-en-1-one having differesnt cox-1 and/or cox-2 selectivities, have been examined on human hepatocarcinoma (hepg2), lung carcinoma (a549), and breast adenocarcinoma (mcf-7) cell line, using sulforhodamine b (srb) assay. briefly, cells were treated with 1-100 µm of each compound for 72, 96 and 168 hours. in each case, a control row was set with the exposure of cells to compounds-free solvents. median lethal concentration (lc50) values (compared to controls) were calculated using regression fitness analysis on graphpad prism® software. our results show that the subgroup possessing p-azido cox-2 pharmacophore seems to be more cytotoxic, while the cells seem to show more acquired resistance to them and the subgroup possessing a p-meso2nh cox-2 pharmacophore is less cytotoxic, while the cells also acquire less resistance to them. in conclusion, considering the diversity in cox-1 or cox-2 inhibition among these compounds in each group, and also revealing no correlation between cox inhibition selectivity and cell death, it seems that selective inhibition of each isoenzyme doesn’t cause substantial effect on toxicity potency. further studies to determine the main mechanism(s) for these compounds induced cell death are encouraged.

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Journal title:
iranian journal of pharmaceutical research

جلد ۱۳، شماره ۳، صفحات ۹۵۳-۹۵۸

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