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
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
Recently,we found that high concentration of taxol(70μM)induced cell death with cytoplasm vacuolization,the typical characteristic of both paraptosis and oncosis,in human lung carcinoma(ASTC-a-1)cells.This report was...Recently,we found that high concentration of taxol(70μM)induced cell death with cytoplasm vacuolization,the typical characteristic of both paraptosis and oncosis,in human lung carcinoma(ASTC-a-1)cells.This report was designed to further deternine the form of taxo-induced cell death with cytoplasm vacuolization.It is generally coneidered that the cytoplasm vacuolization in oncosis due to the sweling of endoplasmic reticulum(ER),mitochondria,lysosomes and muclei occurs after the loss of mitochondrial mermbrane potential(△ψm).However,flow cytometry(FCM)analysis showed that taxol induced cy toplsm vacuolization preceded the loss of(△ψm).Moreover,taxol treatment did not induce the collapse of microtubule,the ty pical characteristic of oncosis.These data demonstrated that taxol-induced cell death with cytoplasm vacuolization is not onoosis.FCM analysis by Annexin V-FTTC/PI apoptosis detection kit further demoustrated that taxol-induced cell death with cytoplasm vacuolization is not apoptosis.In conclusion,in combination with our recent in ritro and in vito data,this report further demonstrates that high concentration of taxol induces cell death with cytoplasm vacuolization in paraptosis like but not oncosis fashion.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...
文摘Jin Fu 坑口头的液体([标志：看见文本]) 用为补充 qi 和有营养的 yin 的繁体中文药做的，与 qi 和 yin 的缺乏在肺癌根据普通症状被开发。在 Jin Fu 坑组的 96 个盒子， 1 个盒子变得完全宽恕(CR ) 术后疗法， 8 个盒子部分宽恕(PR ) ， 52 个盒子不变化(NC ) ，盖住 63.5% 的 PR + NC。在 Jin Fu 坑正化疗的组的 52 个盒子， 11 个盒子得到了 PR 术后疗法， 26 盒子 NC，盖住 71.2% 的 PR + NC。在化疗组的 25 个盒子， 4 个盒子得到了 PR 术后疗法， 11 盒子 NC，盖住 60.0% 的 PR + NC。在 Jin Fu 坑的治疗学的有效性组织的结果表演和 Jin Fu 坑正化疗的组在化疗组比那好。在 Jin Fu 坑组的一个年幸存率和二年的幸存率术后疗法分别地是 67.3% 和 67.3% ；66.7% 和 66.7% 在 Jin Fu 坑正化疗的组；并且 40.3% 和 0.0% 在化疗组织。临床的症状的改进，体重的增加和健康状况(KPS 标记) 的改进 Jin Fu 坑组织的在两个的术后疗法和 Jin Fu 坑正化疗的组在化疗组比那好。免疫学和血克术后疗法的一些指示物极大地在 Jin Fu 坑组，被改进在化疗组，而是在 Jin Fu 坑正化疗的组的没有明显的改进更坏。
基金supported by National Natural Sci-ence Foundation of China(31071218 and 81071491)Key Project of the Department of Education and Finance of Guangdong Province(cxzd115).
文摘Recently,we found that high concentration of taxol(70μM)induced cell death with cytoplasm vacuolization,the typical characteristic of both paraptosis and oncosis,in human lung carcinoma(ASTC-a-1)cells.This report was designed to further deternine the form of taxo-induced cell death with cytoplasm vacuolization.It is generally coneidered that the cytoplasm vacuolization in oncosis due to the sweling of endoplasmic reticulum(ER),mitochondria,lysosomes and muclei occurs after the loss of mitochondrial mermbrane potential(△ψm).However,flow cytometry(FCM)analysis showed that taxol induced cy toplsm vacuolization preceded the loss of(△ψm).Moreover,taxol treatment did not induce the collapse of microtubule,the ty pical characteristic of oncosis.These data demonstrated that taxol-induced cell death with cytoplasm vacuolization is not onoosis.FCM analysis by Annexin V-FTTC/PI apoptosis detection kit further demoustrated that taxol-induced cell death with cytoplasm vacuolization is not apoptosis.In conclusion,in combination with our recent in ritro and in vito data,this report further demonstrates that high concentration of taxol induces cell death with cytoplasm vacuolization in paraptosis like but not oncosis fashion.
