2007Shanghai yixueRequires access

In vitro study on Anthracycline-induced injury of cardiomyocyte H9c2

HE Be

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Abstract

Objective To investigate the anthracycline-induced injury of cardiomyocyte H9c2 cells. Methods H9c2 cells of new born rats were cultured with Daunorubicin(DNR)on the 3~(rd) day of passaging.To measure overall cell injury,we assayed the activity of lactate dehydrogenase(LDH)released into the medium after DNR treatment and the secretion of LDH was determined for evaluation of injury to cell membrane.The in vitro anti-proliferative effect of DNR on H9c2 cells was determined by MTT assay.Cell apoptosis rate was measured by flow cytometry.Results The inhibitory rates of H9c2 ceils in DNR1 group,DNR2 group,and DNR3 groups were (24.93±1.52)%,(17.15±2.03)% and(13.48±2.26)%,respectively,with significant difference found between the 3 groups (all P0.01);the concentrations of LDH in the supernatants were(77.00±6.24), (64.3±10.50)and(57.67±7.24)U,respectively,all significantly higher than that of the blank control group (37.00±6.56)U,all P0.01);the apoptosis rates of H9c2 cells in the 3 groups were(15.47±2.46)%, (9.82±2.08)% and(9.43±1.63)%,respectively,all significantly higher than that of the blank control group (4.49±2.96)%,all P0.05).Conclusion DNR can inhibit proliferation of H9c2 cells,induce cells apoptosis and impair cellular membrane.(Shanghai Med J,2007,30:696-698)

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Objective To investigate the anthracycline-induced injury of cardiomyocyte H9c2 cells. Methods H9c2 cells of new born rats were cultured with Daunorubicin(DNR)on the 3~(rd) day of passaging.To measure overall cell injury,we assayed the activity of lactate dehydrogenase(LDH)released into the medium after DNR treatment and the secretion of LDH was determined for evaluation of injury to cell membrane.The in vitro anti-proliferative effect of DNR on H9c2 cells was determined by MTT assay.Cell apoptosis rate was measured by flow cytometry.Results The inhibitory rates of H9c2 ceils in DNR1 group,DNR2 group,and DNR3 groups were (24.93±1.52)%,(17.15±2.03)% and(13.48±2.26)%,respectively,with significant difference found between the 3 groups (all P0.01);the concentrations of LDH in the supernatants were(77.00±6.24), (64.3±10.50)and(57.67±7.24)U,respectively,all significantly higher than that of the blank control group (37.00±6.56)U,all P0.01);the apoptosis rates of H9c2 cells in the 3 groups were(15.47±2.46)%, (9.82±2.08)% and(9.43±1.63)%,respectively,all significantly higher than that of the blank control group (4.49±2.96)%,all P0.05).Conclusion DNR can inhibit proliferation of H9c2 cells,induce cells apoptosis and impair cellular membrane.(Shanghai Med J,2007,30:696-698)

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Available abstract

Objective To investigate the anthracycline-induced injury of cardiomyocyte H9c2 cells. Methods H9c2 cells of new born rats were cultured with Daunorubicin(DNR)on the 3~(rd) day of passaging.To measure overall cell injury,we assayed the activity of lactate dehydrogenase(LDH)released into the medium after DNR treatment and the secretion of LDH was determined for evaluation of injury to cell membrane.The in vitro anti-proliferative effect of DNR on H9c2 cells was determined by MTT assay.Cell apoptosis rate was measured by flow cytometry.Results The inhibitory rates of H9c2 ceils in DNR1 group,DNR2 group,and DNR3 groups were (24.93±1.52)%,(17.15±2.03)% and(13.48±2.26)%,respectively,with significant difference found between the 3 groups (all P0.01);the concentrations of LDH in the supernatants were(77.00±6.24), (64.3±10.50)and(57.67±7.24)U,respectively,all significantly higher than that of the blank control group (37.00±6.56)U,all P0.01);the apoptosis rates of H9c2 cells in the 3 groups were(15.47±2.46)%, (9.82±2.08)% and(9.43±1.63)%,respectively,all significantly higher than that of the blank control group (4.49±2.96)%,all P0.05).Conclusion DNR can inhibit proliferation of H9c2 cells,induce cells apoptosis and impair cellular membrane.(Shanghai Med J,2007,30:696-698)

Key concepts: Lactate dehydrogenase, Daunorubicin, Apoptosis, Flow cytometry, Medicine, In vitro, Molecular biology, Anthracycline

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