茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

茶多酚通过调节Akt通路诱导胰腺癌细胞凋亡

Objective To investigate the regulation of Akt signaling pathway involved in apeptosis of Panc-I cells induced by polyphenol ( - )-epigallocatechin-3-gallate. Methods Pane-1 cells were maintained in DMEM with 10% fetal calf serum in a 95% air,5% CO2 atmosphere,then incubated in different concentrations of EGCG (6.3,12.5,25.0,50.0 μmol/L). The growth arrest effect was determined by MTT assay, and apoptosis was detected by agarose gel electrophoresis. The levels of Akt (60×103 ) and Bad (23×103) were determined by Western blot. Results EGCG time and dose dependently repressed the growth of Panc-1 cells and induced apeptosis in Panc-1 cells ( P <0.05 ). The expression of p-Akt (set473) and p-Bad (ser136) was reduced in a dose-dependent way,whereas the pan-Akt and pan-Bad were unchanged (P < 0.05). Conclusion EGCG can induce apoptosis in pancreatic cancer cells in a dose-and time-dependent fashion by attenuating the blocking effects of Akt signaling pathway on Bad proteins.     

靶向Survivin的siRNA联合吉西他滨抑制胰腺癌细胞增殖

Objective To construct the siRNA eukaryotic expression vector targeting Survivin gene, and investigate the chemotherapy sensitivity of pancreatic cancer line Panc-1 treated by gemcitabine. Methods The siRNA eukaryotic expression vector targeting Survivin gene was constructed. Panc-1 cells were transfected with negative control vector or siRNA vector and selected by G418, and the cell growth curve was drawn. The expression of Survivin mRNA and protein was detected by RT-PCR and Western blot respectively. Panc-1 cells or transfected cells were treated with gemcitabine for 24 h,and then the growth inhibition rate was measured by MTT assay, and cell apeptosis rate was measured by flow cytometry. Results The result of endonuclease digestion and DNA sequencing revealed that the recombinant plasmid psiRNA-Survivin was constructed successfully. Survivin mRNA and protein levels were reduced by 79.2% and 83.6% respectively in stably transfected Panc-1 cells as compared with control group, and the cell growth curve was much smoother, and the growth inhibition rate [ ( 24.6±4.5 ) % / (38.7±5.2 ) % ] and apoptosis rate of these cells [ ( 16.7±2.5 ) %/( 26.8±3.4 ) % ] were significantly increased after treatment by gemcitabine (P < 0.05 ). Conclusion The constructed siRNA eukaryotie expression vector targeting Survivin could decrease the Survivin expression,inhibit the growth of Panc-1 cells significantly,and increase the chemotherapy sensitivity to gemcitabine.     

Faculty of Anaesthetists of the Royal College of Surgeons of Ireland

The Faculty of Anaesthetists of the Royal College of Surgeons of England, 35–43 Lincoln's Inn Fields, London WC2A 3PN. Telephone: 01-405 3474.     

深圳市某两所小学流行性腮腺炎突发疫情的流行病学分析

目的：通过对深圳市某两所小学发生的流行性腮腺炎突发疫情的流行病学特点及差异性进行分析,为制定科学、高效的防控策略提供科学依据。方法2013年5～7月深圳市大鹏新区某两所小学爆发流行性腮腺炎,以学校为整体研究对象,分别标记为学校A（24个班,学生1210例）和学校B（27个班,学生1274例）,对比两所小学的疫情流行病学差异性。结果分析发现,学校A流行性腮腺炎发病率为4.30%,发病班级所占比54.17%,均较学校B1.73%和29.63%高,对比差异有统计学意义（P＜0.05）;分析显示学校A学生出现疫病平均年龄为（11.2±1.1）岁,较学校B（9.34±1.0）岁,对比差异明显（P＜0.05）;且两组疫病患儿在接种疫苗率对比上差异无统计学意义（P＞0.05）;但疫情发生时,学校B疫苗紧急接种率明显高于学校A,对比差异有统计学意义（P＜0.05）。结论小学作为流行性腮腺炎爆发的主要场所之一,疫病爆发高峰季节前,针对易感染人群给予相应的疫苗接种等预防控制措施,同时加强流行性腮腺炎的监测,对于降低感染人群数量,减轻、遏制疫情有着积极的意义,值得相关防控部门重视。