CAJ | 학술논문

该文观察ECG在人鼻咽癌细胞株C666-1增殖与凋亡中的作用，并初步探讨其机制．人鼻咽癌C666-1细胞给予不同浓度ECG（0～100μmol／L）处理48 h后，采用CCK-8法检测细胞增殖水平，使用TUNEL法和流式细胞仪检测细胞凋亡率，利用Western blotting法检测Bax、Bcl-2、Caspase 3等凋亡相关蛋白的表达变化．结果表明，25μmol／L以上浓度的ECG可抑制C666-1细胞增殖，诱导细胞凋亡；并且ECG可浓度依赖性增加Bax／Bcl-2蛋白比值和剪切的Caspase 3蛋白水平．以上结果表明ECG可抑制人鼻咽癌细胞株C666-1增殖，并诱导细胞凋亡．ECG的作用与其增加Bax／Bcl-2相对蛋白比值进而激活caspase-3有关．
해문관찰ECG재인비인암세포주C666-1증식여조망중적작용，병초보탐토기궤제．인비인암C666-1세포급여불동농도ECG（0～100μmol／L）처리48 h후，채용CCK-8법검측세포증식수평，사용TUNEL법화류식세포의검측세포조망솔，이용Western blotting법검측Bax、Bcl-2、Caspase 3등조망상관단백적표체변화．결과표명，25μmol／L이상농도적ECG가억제C666-1세포증식，유도세포조망；병차ECG가농도의뢰성증가Bax／Bcl-2단백비치화전절적Caspase 3단백수평．이상결과표명ECG가억제인비인암세포주C666-1증식，병유도세포조망．ECG적작용여기증가Bax／Bcl-2상대단백비치진이격활caspase-3유관．
The effect of ECG on the proliferation and apoptosis of nasopharyngeal carcinoma cell line C666-1 were studied.C666-1 cells were treated with different concentrations (0~100 μmol/L) of ECG for 48 h, CCK-8 assay was used to evaluate the proliferation.TUNEL assay and Flow Cytometric Analysis were used to investigate the ap-optosis of C666-1 cells.Western blotting was performed to detect the expression level of Bax, Bcl-2 and Caspase 3. ECG above 25μmol/L could inhibit the proliferation, induce the apoptosis of C666-1 cells, and upregulate the lev-els of Bax/Bcl-2 and cleaved caspase 3.ECG could inhibit proliferation and induce apoptosis of nasopharyngeal carcinoma cell line C666-1 by regulating Bax-Bcl-2-Caspase 3 signaling pathway.