【摘要】 目的撤血清培养舌鳞癌细胞TCA-8113模拟舌苔细胞凋亡过程,过氧化氢（hydrogen dioxide,H₂O₂）刺激探讨氧化应激影响舌苔形成相关细胞模型凋亡的分子机制。方法撤血清培养舌鳞癌细胞TCA-8113,H₂O₂作用舌鳞癌细胞TCA-8113模拟氧化应激,MTT法检测细胞增殖活性,PI染色结合流式细胞术检测细胞周期,Annexin V-FITC细胞凋亡检测,蛋白免疫印迹（western blot）检测蛋白表达,ELISA检测培养上清PGE2含量。结果 H₂O₂作用后,撤血清舌鳞癌TCA-8113细胞增殖活性显著下降并具有剂量和时间依赖性;细胞周期分布变化显著,促进细胞凋亡;下调撤血清舌鳞癌细胞NF-κB p50、Bcl-2和Bax的表达水平,上调撤血清舌鳞癌细胞NF-κB p65和COX-2的表达水平;同时,舌鳞癌细胞PGE2分泌量也表现为剂量依赖效应。结论氧化应激可以促进舌苔形成相关细胞凋亡。更多还原

【Abstract】 Objective To investigate the mechanism of oxidative stress on inducing apoptosis related to the formation of tongue coating. Methods The TCA-8113 cells were treated by hydrogen dioxide（H₂O₂） in the different doses for different time. The proliferative activity was detected by MTT method. The flow cytometric analysis was conducted to analyze the cell cycle distribution（PI） and apoptosis（Annexin V-FITC）. The expressions of NF-κB p50,NF-κB p65,COX-2,Bcl-2 and Bax were analyzed by Western blotting. The level of the PGE2 was detected by ELISA. Result H₂O₂ obviously inhibited the proliferative activity of TCA-8113 cells with serum withdrawal. H₂O₂ had influence on the distribution of cell cycle,promoted apoptosis and high level of PGE2 of TCA-8113 cells with serum withdrawal.H₂O₂ significantly regulated downward the expression of NF-κB p50 and upward the expressions of NF-κB p65,COX-2. H₂O₂（10 μmol/L） obviously regulated downward the expression of Bcl-2,Bax. Conclusion H₂O₂ could promote apoptosis related to the formation of tongue coating.更多还原