Objective： To investigate the effect of paclitaxel on cell proliferation and apoptosis of human lung adenocarcinoma A549 cells line and its mechanism in vitro. Methods ： Cell growth inhibition of paclitaxel on A549 ...Objective： To investigate the effect of paclitaxel on cell proliferation and apoptosis of human lung adenocarcinoma A549 cells line and its mechanism in vitro. Methods ： Cell growth inhibition of paclitaxel on A549 cells was analyzed by MTT assay. Cell apoptosis was detected by DNA cytofluorometry, Hoechst33258 staining when treated with paclitaxel for 48 hours. Meanwhile, Cell cycle and apoptotic rate were analyzed by flow cytometry. The protein expressions of Bax and Bcl-2 were studied by Western Blot. Results： Paclitaxel inhibited the proliferation of A549 cells in a time-and dose-dependant manner. Hoechst33258 staining indicated that apoptosis was induced by paclitaxel. After treated for 48 hours, cell apoptosis rates of 25 nmo1/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 11.52 ± 1.94% ,17.73 ±2.53%, and 29.32 ±5.51% respectively, which were significantly higher than those of control group 5.88 ±1.07%（all P 〈 0.01 ）, and apoptosis rate increased in dose-dependant manner. Meanwhile, G2/M stage cell percentage of 25 nmol/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 42.52 ± 6.25%, 40.46 ± 5.81%, and 35.34 ±6.17% respectively,which were significantly higher than that of control group 22.32 ± 3.30%（all P 〈 0.01 ）; Western blot showed that paclitaxel increased the expression of Bax and decreased the expression of Bcl-2 in dose-dependant manner. Conclusion： Paclitaxel can inhibit A549 cell proliferation in a time-and dose-dependant manner. Its mechanism may be related to arresting cell cycle in G2/M stage and induce cell apoptosis by up-modulating Bax expression and down-modulating Bcl-2 expression.展开更多
Lung cancer is one of the serious threats to human health and life of malignant diseases, on a global scale; it has become one of the major lung cancer deaths. Due to the growth of the tumor and the main reason is tha...Lung cancer is one of the serious threats to human health and life of malignant diseases, on a global scale; it has become one of the major lung cancer deaths. Due to the growth of the tumor and the main reason is that apoptosis is inhibited, therefore, it can induce apoptosis in lung cancer cells that is an important measure for the treatment of lung cancer, which is one of the effective means to reduce lung cancer mortality. In this paper, A549 human lung adenocarcinoma cell line, for example, has the use of chemical genetics of these emerging technological platforms, research pravastatin on apoptosis in human lung adenocarcinoma A549 intervention, while providing a theoretical basis for the development of new lung cancer therapy.展开更多
In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantatio...In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adenocarcinoma were established.When the largest diameter of tumor reached 1.0cm,all nude mice were randomly divided into 4 groups:Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest d...展开更多
Objective:The aim of the study was to investigate the effect of Demethyl bryoanthrathiophene(DBT) on proliferations of human umbilical vein endothelial cells(HUVECs) and human lung adenocarcinoma cell line A549,and an...Objective:The aim of the study was to investigate the effect of Demethyl bryoanthrathiophene(DBT) on proliferations of human umbilical vein endothelial cells(HUVECs) and human lung adenocarcinoma cell line A549,and antiangiogenic effect of DBT on HUVECs in vitro.Methods:MTT assay was used to observe the effect of DBT on proliferations of HUVECs and A549 cells,flat plate scarification assay and tube formation in vitro test were used to observe the impact of DBT on migration and vaso-formed ability of HUVECs.The effects of DBT on apoptosis and cell cycle of HUVECs were calculated by flow cytometry.Results:MTT assay showed that treatment with DBT resulted in strong inhibition to the growth of HUVECs and A549 cells.The inhibition effects of DBT on HUVECs and A549 cells were related to dosage and times of dependency.In different doses of DBT(0.16,0.32 and 0.48 μmol/L) of flat plate scarification for 24 h,inhibition rates of DBT to migration of HUVECs were 14.70%,38.23% and 58.82%,respectively.In dose of DBT from 0.04,0.20 to 0.40 μmol/L for 24 h in tube formation,there were significance differences(P < 0.01) in the decreasing number of angiogenesis and incomplete blood vessel compared with control groups.All results showed that DBT promoted the apoptosis rate of HUVECs,and the increase of concentration of DBT accompanied the acceleration of apoptosis rate.Conclusion:DBT could inhibit the proliferations of HUVECs and A549 cells,and effectively suppress angiogenesis in vitro.展开更多
文摘Objective： To investigate the effect of paclitaxel on cell proliferation and apoptosis of human lung adenocarcinoma A549 cells line and its mechanism in vitro. Methods ： Cell growth inhibition of paclitaxel on A549 cells was analyzed by MTT assay. Cell apoptosis was detected by DNA cytofluorometry, Hoechst33258 staining when treated with paclitaxel for 48 hours. Meanwhile, Cell cycle and apoptotic rate were analyzed by flow cytometry. The protein expressions of Bax and Bcl-2 were studied by Western Blot. Results： Paclitaxel inhibited the proliferation of A549 cells in a time-and dose-dependant manner. Hoechst33258 staining indicated that apoptosis was induced by paclitaxel. After treated for 48 hours, cell apoptosis rates of 25 nmo1/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 11.52 ± 1.94% ,17.73 ±2.53%, and 29.32 ±5.51% respectively, which were significantly higher than those of control group 5.88 ±1.07%（all P 〈 0.01 ）, and apoptosis rate increased in dose-dependant manner. Meanwhile, G2/M stage cell percentage of 25 nmol/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 42.52 ± 6.25%, 40.46 ± 5.81%, and 35.34 ±6.17% respectively,which were significantly higher than that of control group 22.32 ± 3.30%（all P 〈 0.01 ）; Western blot showed that paclitaxel increased the expression of Bax and decreased the expression of Bcl-2 in dose-dependant manner. Conclusion： Paclitaxel can inhibit A549 cell proliferation in a time-and dose-dependant manner. Its mechanism may be related to arresting cell cycle in G2/M stage and induce cell apoptosis by up-modulating Bax expression and down-modulating Bcl-2 expression.
文摘Lung cancer is one of the serious threats to human health and life of malignant diseases, on a global scale; it has become one of the major lung cancer deaths. Due to the growth of the tumor and the main reason is that apoptosis is inhibited, therefore, it can induce apoptosis in lung cancer cells that is an important measure for the treatment of lung cancer, which is one of the effective means to reduce lung cancer mortality. In this paper, A549 human lung adenocarcinoma cell line, for example, has the use of chemical genetics of these emerging technological platforms, research pravastatin on apoptosis in human lung adenocarcinoma A549 intervention, while providing a theoretical basis for the development of new lung cancer therapy.
文摘In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adenocarcinoma were established.When the largest diameter of tumor reached 1.0cm,all nude mice were randomly divided into 4 groups:Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest d...
基金Supported by a grant from the National Natural Science Foundation of China (No.30472078)
文摘Objective:The aim of the study was to investigate the effect of Demethyl bryoanthrathiophene(DBT) on proliferations of human umbilical vein endothelial cells(HUVECs) and human lung adenocarcinoma cell line A549,and antiangiogenic effect of DBT on HUVECs in vitro.Methods:MTT assay was used to observe the effect of DBT on proliferations of HUVECs and A549 cells,flat plate scarification assay and tube formation in vitro test were used to observe the impact of DBT on migration and vaso-formed ability of HUVECs.The effects of DBT on apoptosis and cell cycle of HUVECs were calculated by flow cytometry.Results:MTT assay showed that treatment with DBT resulted in strong inhibition to the growth of HUVECs and A549 cells.The inhibition effects of DBT on HUVECs and A549 cells were related to dosage and times of dependency.In different doses of DBT(0.16,0.32 and 0.48 μmol/L) of flat plate scarification for 24 h,inhibition rates of DBT to migration of HUVECs were 14.70%,38.23% and 58.82%,respectively.In dose of DBT from 0.04,0.20 to 0.40 μmol/L for 24 h in tube formation,there were significance differences(P < 0.01) in the decreasing number of angiogenesis and incomplete blood vessel compared with control groups.All results showed that DBT promoted the apoptosis rate of HUVECs,and the increase of concentration of DBT accompanied the acceleration of apoptosis rate.Conclusion:DBT could inhibit the proliferations of HUVECs and A549 cells,and effectively suppress angiogenesis in vitro.
