Tea polyphenols have been shown to have anticancer activity in many studies.In the present study,we investigated effects of theaflavin-3-3'-digallate(TF3),one of the major theaflavin monomers in black tea,in combi...Tea polyphenols have been shown to have anticancer activity in many studies.In the present study,we investigated effects of theaflavin-3-3'-digallate(TF3),one of the major theaflavin monomers in black tea,in combination with ascorbic acid(AA),a reducing agent,and(-)-epigallocatechin-3-gallate(EGCG),the main polyphenol presented in green tea,in combination with AA on cellular viability and cell cycles of the human lung adenocarcinoma SPC-A-1 cells.The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) assay showed that the 50% inhibition concentrations(IC50) of TF3,EGCG,and AA on SPC-A-1 cells were 4.78,4.90,and 30.62 μmol/L,respectively.The inhibitory rates of TF3 combined with AA(TF3+AA) and EGCG combined with AA(EGCG+AA) at a molar ratio of 1:6 on SPC-A-1 cells were 54.4% and 45.5%,respectively.Flow cytometry analysis showed that TF3+AA and EGCG+AA obviously increased the cell population in the G0/G1 phase of the SPC-A-1 cell cycle from 53.9% to 62.8% and 60.0%,respectively.TF3-treated cells exhibited 65.3% of the G0/G1 phase at the concentration of its IC50.Therefore,TF3+AA and EGCG+AA had synergistic inhibition effects on the proliferation of SPC-A-1 cells,and significantly held SPC-A-1 cells in G0/G1 phase.The results suggest that the combination of TF3 with AA or EGCG with AA enhances their anticancer activity.展开更多
目的:评价表没食子儿茶素没食子酸酯(EGCG)及其甲基化修饰物(EGCG-3Me)改性粘接剂对根管牙本质粘接界面稳定性的作用。方法:将质量浓度为400μg/ml的EGCG及EGCG-3Me添加到全酸蚀粘接剂Single Bond 2(SB2)中,制备改性粘接剂E-SB2及E3-SB2...目的:评价表没食子儿茶素没食子酸酯(EGCG)及其甲基化修饰物(EGCG-3Me)改性粘接剂对根管牙本质粘接界面稳定性的作用。方法:将质量浓度为400μg/ml的EGCG及EGCG-3Me添加到全酸蚀粘接剂Single Bond 2(SB2)中,制备改性粘接剂E-SB2及E3-SB2,SB2为对照组。激光共聚焦显微镜和分光光度法检测改性粘接剂抗粪肠球菌的性能。微拉曼光谱仪检测粘接剂双键转化率。制备纤维桩粘接试件,用于即刻和老化后的微推出实验。结果:改性粘接剂可以抑制粪肠球菌生物膜形成,且EGCG-3Me作用更显著。改性粘接剂与SB2的双键转化率和即刻微推出粘接强度差异无显著性(P>0.05)。老化后改性粘接剂的微推出粘接强度显著高于SB2(P<0.05)。结论:EGCG和EGCG-3Me改性的粘接剂均可抑制粪肠球菌增殖并提高树脂-根管牙本质粘接界面稳定性,EGCG-3Me抗菌性能较佳。展开更多
AIM:(-)-Epigallocatechin-3-gallate(EGCG), a major compound of tea polyphenols, exhibited antitumor activity in previous studies. In these studies, EGCG usually inhibits EGFR, and impairs the ERK1/2 phosphorylation in ...AIM:(-)-Epigallocatechin-3-gallate(EGCG), a major compound of tea polyphenols, exhibited antitumor activity in previous studies. In these studies, EGCG usually inhibits EGFR, and impairs the ERK1/2 phosphorylation in tumor cells. The aim was to clarify the mechanism of ERK1/2 activation induced by EGCG. METHODS: Jurkat and 293 T cells were treated with EGCG in different culture conditions. Western Blotting(WB) was employed to analyze ERK1/2 and MEK phosphorylation. Cetuximab and FR180204 were used to inhibit cell signaling. The stability of EGCG was assessed by HPLC. The concentration of hydrogen peroxide generated by the auto-oxidation of EGCG was determined by photocolorimetric analysis. RESULTS: Activation of ERK1/2 was observed to be both time- and dose-dependent. Stimulation of cell signaling was dependent on MEK activity, but independent of EGFR activity. Unexpectedly, EGCG was depleted within one hour of incubation under traditional culture conditions. Auto-oxidation of EGCG generated a high level of hydrogen peroxide in the medium. Addition of catalase and SOD to the acidic medium inhibited the oxidation of EGCG. However, this particular condition also prevented the phosphorylation of ERK1/2. The generation of ROS by hydrogen peroxide may also induce ERK1/2 activation in Jurkat cells. CONCLUSION: ERK1/2 phosphorylation was caused by auto-oxidation of EGCG. Traditional culture conditions were determined to be inappropriate for EGCG research.展开更多
基金supported by the Key Program of Science and Technology of Zhejiang Province(No.2007C12068)of Chinathe National Natural Science Foundation of China(No.30901002)
文摘Tea polyphenols have been shown to have anticancer activity in many studies.In the present study,we investigated effects of theaflavin-3-3'-digallate(TF3),one of the major theaflavin monomers in black tea,in combination with ascorbic acid(AA),a reducing agent,and(-)-epigallocatechin-3-gallate(EGCG),the main polyphenol presented in green tea,in combination with AA on cellular viability and cell cycles of the human lung adenocarcinoma SPC-A-1 cells.The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) assay showed that the 50% inhibition concentrations(IC50) of TF3,EGCG,and AA on SPC-A-1 cells were 4.78,4.90,and 30.62 μmol/L,respectively.The inhibitory rates of TF3 combined with AA(TF3+AA) and EGCG combined with AA(EGCG+AA) at a molar ratio of 1:6 on SPC-A-1 cells were 54.4% and 45.5%,respectively.Flow cytometry analysis showed that TF3+AA and EGCG+AA obviously increased the cell population in the G0/G1 phase of the SPC-A-1 cell cycle from 53.9% to 62.8% and 60.0%,respectively.TF3-treated cells exhibited 65.3% of the G0/G1 phase at the concentration of its IC50.Therefore,TF3+AA and EGCG+AA had synergistic inhibition effects on the proliferation of SPC-A-1 cells,and significantly held SPC-A-1 cells in G0/G1 phase.The results suggest that the combination of TF3 with AA or EGCG with AA enhances their anticancer activity.
文摘目的:评价表没食子儿茶素没食子酸酯(EGCG)及其甲基化修饰物(EGCG-3Me)改性粘接剂对根管牙本质粘接界面稳定性的作用。方法:将质量浓度为400μg/ml的EGCG及EGCG-3Me添加到全酸蚀粘接剂Single Bond 2(SB2)中,制备改性粘接剂E-SB2及E3-SB2,SB2为对照组。激光共聚焦显微镜和分光光度法检测改性粘接剂抗粪肠球菌的性能。微拉曼光谱仪检测粘接剂双键转化率。制备纤维桩粘接试件,用于即刻和老化后的微推出实验。结果:改性粘接剂可以抑制粪肠球菌生物膜形成,且EGCG-3Me作用更显著。改性粘接剂与SB2的双键转化率和即刻微推出粘接强度差异无显著性(P>0.05)。老化后改性粘接剂的微推出粘接强度显著高于SB2(P<0.05)。结论:EGCG和EGCG-3Me改性的粘接剂均可抑制粪肠球菌增殖并提高树脂-根管牙本质粘接界面稳定性,EGCG-3Me抗菌性能较佳。
基金supported by the Natural Science Foundation of Yunnan Province,China(No.2012FB151)
文摘AIM:(-)-Epigallocatechin-3-gallate(EGCG), a major compound of tea polyphenols, exhibited antitumor activity in previous studies. In these studies, EGCG usually inhibits EGFR, and impairs the ERK1/2 phosphorylation in tumor cells. The aim was to clarify the mechanism of ERK1/2 activation induced by EGCG. METHODS: Jurkat and 293 T cells were treated with EGCG in different culture conditions. Western Blotting(WB) was employed to analyze ERK1/2 and MEK phosphorylation. Cetuximab and FR180204 were used to inhibit cell signaling. The stability of EGCG was assessed by HPLC. The concentration of hydrogen peroxide generated by the auto-oxidation of EGCG was determined by photocolorimetric analysis. RESULTS: Activation of ERK1/2 was observed to be both time- and dose-dependent. Stimulation of cell signaling was dependent on MEK activity, but independent of EGFR activity. Unexpectedly, EGCG was depleted within one hour of incubation under traditional culture conditions. Auto-oxidation of EGCG generated a high level of hydrogen peroxide in the medium. Addition of catalase and SOD to the acidic medium inhibited the oxidation of EGCG. However, this particular condition also prevented the phosphorylation of ERK1/2. The generation of ROS by hydrogen peroxide may also induce ERK1/2 activation in Jurkat cells. CONCLUSION: ERK1/2 phosphorylation was caused by auto-oxidation of EGCG. Traditional culture conditions were determined to be inappropriate for EGCG research.
