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Chinese Journal of Natural Medicines 2016-Mar

In vitro antiproliferative and apoptosis-inducing activities of crude ethyle alcohole extract of Quercus brantii L. acorn and subsequent fractions.

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Mohammad-Taghi Moradi
Ali Karimi
Somayeh Alidadi

Клучни зборови

Апстракт

Cancer cell resistance to widely used chemotherapeutic agents is gradually developed. Natural products, mainly isolated from medicinal plants, have been considered as valuable sources for herbal anticancer drugs. The present study aimed to evaluate in vitro antiproliferative and apoptosis-inducing activities of crude ethyle alcohole extract and four fractions of Q. brantii acorn. Crude ethyle alcohole extract of Q. brantii acorn was prepared and subjected to fractionation with different polarity. Subsequently, the extract and the fractions wereevaluated for their in vitro antiproliferative activity in two cancerous (Hela and AGS) and one normal (HDFs) cell lines using MTT [3-(4, 5-dimethylthiazol-2ol) 2, 5 diphenyltetrazoliumbromide] assay. To determine whether the cytotoxicity of these compounds involved the induction of apoptosis, Hela cells were treated with IC50 concentrations of test compounds, stained with both propidium iodide (PI) and Annexin V-fluorescein isothiocyanate (FITC), and analyzed by flow cytometry. In vitro cytotoxicity assay showed that the cell viability was significantly reduced in a dose-dependent manner following treatment with crude ethyle alcohole extract and Cholophorm and n-Butanol fractions. Based on the probit regression model, antiproliferative activities of crude ethyle alcohole extract, Cholophorm fraction, and n-Butanol fraction on Hela and AGS cells and HDFs cells were significantly different (P < 0.001). The results of flow cytometric analysis showed that crude ethyle alcohole extract and two fractions of Q. brantii acorn induced early apoptotic cell death. These findings suggest that crude ethyle alcohole extract and Cholophorm and n-Butanol fractions of Q. brantii acorn suppress the proliferation of cancer cells through induction of early apoptosis.

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