CAJ | 학술논문

目的观察矢车菊素-3-葡萄糖苷(C3G)在体外诱导人胃癌SGC7901细胞凋亡的生物学效应,并初步探讨其分子机制.方法分别采用不同浓度梯度的C3G处理SGC7901胃癌细胞,MTT比色法检测细胞生长率；激光共聚焦显微镜观察细胞形态改变；TUNEL法分析细胞凋亡率；Western blot法检测凋亡相关基因Bcl-2、Bax、Caspase-3、ICAD蛋白表达的情况.结果 C3G在体外能明显抑制人胃癌SGC7901细胞的生长增殖,且呈浓度、时间依赖性(P＜0.01).激光共聚焦显微镜下可见Hoechst33258荧光染色细胞呈凋亡特征性改变；TUNEL法检测实验组细胞凋亡率均明显高于阴性对照组(P＜0.01)；C3G可下调Bcl-2蛋白表达,上调Bax蛋白表达,降低Bcl-2/Bax蛋白的比值,促使Caspase-3酶原蛋白活化,下调ICAD蛋白表达(P＜0.01).结论 C3G具有在体外抑制胃癌细胞增殖的作用,并能诱导其凋亡,其机制可能与Bcl-2/Bax降低导致Caspase-3活化、ICAD蛋白表达下降相关.
목적 관찰시차국소-3-포도당감(C3G)재체외유도인위암SGC7901세포조망적생물학효응,병초보탐토기분자궤제.방법 분별채용불동농도제도적C3G처리SGC7901위암세포,MTT비색법검측세포생장솔；격광공취초현미경관찰세포형태개변；TUNEL법분석세포조망솔；Western blot법검측조망상관기인Bcl-2、Bax、Caspase-3、ICAD단백표체적정황.결과 C3G재체외능명현억제인위암SGC7901세포적생장증식,차정농도、시간의뢰성(P＜0.01).격광공취초현미경하가견Hoechst33258형광염색세포정조망특정성개변；TUNEL법검측실험조세포조망솔균명현고우음성대조조(P＜0.01)；C3G가하조Bcl-2단백표체,상조Bax단백표체,강저Bcl-2/Bax단백적비치,촉사Caspase-3매원단백활화,하조ICAD단백표체(P＜0.01).결론 C3G구유재체외억제위암세포증식적작용,병능유도기조망,기궤제가능여Bcl-2/Bax강저도치Caspase-3활화、ICAD단백표체하강상관.
Objective To investigate the effect of cyanidin-3-glucopyranoside extracted from Chinese bayberry on proliferation and apoptosis of human gastric cell line SGC7901.Methods After cocultured with C3G on different concentrations,cell proliferation was determined by MTT assay; morphology of apoptosis were observed by laser confocal microscopy; TUNEL assay was applied to measure the apoptoic rate; The expression of Bcl-2,Bax,Caspase-3,ICAD protein were observed by Western blot assay.Results C3G significantly inhibited the proliferation of SGC7901 cells in a concentration-and timedependent manner as measured by MTT method(P ＜ 0.01).After cells were treated with C3G,the presence of typical morphological changes of apoptosis was confirmed with laser confocal microscopy after Hoechst 33258 fluorescence staining.TUNEL assay indicated that the number of apoptotic cells in C3G-treated group was greater than that in the gastric cancer cells group(P ＜ 0.01).The expression level of Bcl-2 was down-regulated while the expression level of Bax was up-regulated by C3G,the ratio of Bcl-2 protein and Bax protein decreased.C3G may accelerate the activation of procaspase-3 and down-regulate the expression of ICAD(P ＜ 0.01).Conclusions C3G inhibits SGC7901 cell growth and induces apoptosis in a concentraion-and time-dependent manner.This action may be mediated by down-regulating Bcl-2/Bax,resulting in Caspase-3 activition and decreased ICAD protein expression.