Pterostilbene Enhances Anticancer Effects of L-asparaginase in Lymphoblastic Leukaemia Cell Line
By: Rahimnejad, T
.
Contributor(s): Beshkar, P.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2019Edition: Vol.81(2), Mar-Apr.Description: 226-233p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
Indian journal of pharmaceutical sciencesSummary: Antiproliferative and apoptotic effects of pterostilbene were examined in combination with L-asparaginase in Jurkat cell line. Jurkat cells were incubated with different concentrations of pterostilbene alone or in combination with L-asparaginase for 24, 48 and 72 h. Cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-5-3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Induction of apoptosis was measured by annexin-V fluorescein isothiocyanate and the level of active caspase 3 positive cells by intracellular staining and flowcytometry. Decline of cell viability to 50 % was observed at 67.78±3.88, 60.97±3.36 and 52.11±2.50 μM concentration after 24, 48 and 72 h incubation with pterostilbene, respectively. Pterostilbene at a concentration of 30, 50 and 70 μM in combination with 0.5 and 0.7 IU/ml L-asparaginase reduced relative cell growth to a significant level. The rate of apoptosis was significantly higher than control at 80 μM concentration of pterostilbene and a combination of 60 μM pterostilbene with 0.5 and 0.7 IU/ml L-asparaginase, but not with L-asparaginase alone. The level of caspase 3 positive cells was significantly higher than control at 80 μM concentration of pterostilbene. Pterostilbene increased antiproliferative and apoptotic effects of L-asparaginase in Jurkat cells. These results suggested that pterostilbene might be a potential anticancer agent in lymphoblastic leukaemia and potentiate the effect of L-asparaginase. Unravelling the mechanism of pterostilbene-induced cell apoptosis in this cell line could help in the development of a targeted therapy
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Antiproliferative and apoptotic effects of pterostilbene were examined in combination with L-asparaginase in Jurkat cell line. Jurkat cells were incubated with different concentrations of pterostilbene alone or in combination with L-asparaginase for 24, 48 and 72 h. Cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-5-3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Induction of apoptosis was measured by annexin-V fluorescein isothiocyanate and the level of active caspase 3 positive cells by intracellular staining and flowcytometry. Decline of cell viability to 50 % was observed at 67.78±3.88, 60.97±3.36 and 52.11±2.50 μM concentration after 24, 48 and 72 h incubation with pterostilbene, respectively. Pterostilbene at a concentration of 30, 50 and 70 μM in combination with 0.5 and 0.7 IU/ml L-asparaginase reduced relative cell growth to a significant level. The rate of apoptosis was significantly higher than control at 80 μM concentration of pterostilbene and a combination of 60 μM pterostilbene with 0.5 and 0.7 IU/ml L-asparaginase, but not with L-asparaginase alone. The level of caspase 3 positive cells was significantly higher than control at 80 μM concentration of pterostilbene. Pterostilbene increased antiproliferative and apoptotic effects of L-asparaginase in Jurkat cells. These results suggested that pterostilbene might be a potential anticancer agent in lymphoblastic leukaemia and potentiate the effect of L-asparaginase. Unravelling the mechanism of pterostilbene-induced cell apoptosis in this cell line could help in the development of a targeted therapy
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