CAJ | 학술논문

目的：探讨杨梅素对人肝癌细胞系 HepG2凋亡的影响及其机制。方法以不同浓度的杨梅素孵育HepG2细胞，在不同时间分别采用倒置显微镜观察细胞形态学变化；采用噻唑蓝（MTT）法检测细胞存活率；采用乳酸脱氢酶（LDH）活力定量测定试剂盒测定细胞上清液LDH活性；采用流式细胞术检测细胞凋亡率；采用蛋白质印迹法检测细胞凋亡途径关键蛋白的表达。结果杨梅素对HepG2细胞的凋亡诱导作用呈现剂量和时间依赖性。杨梅素作用于HepG2细胞，随杨梅素浓度增加，细胞凋亡率增加。与正常对照组相比，100μmol/L杨梅素作用于HepG2细胞24 h后，细胞存活率明显降低[（100.02±5.97）%vs.（71.60±3.75）%，P=0.006]；早、晚期细胞凋亡率明显升高[（10.19±2.61）%vs.（2.52±2.05）%，P=0.003；（11.71±3.34）%vs.（3.69±1.13）%，P=0.004]，差异均有统计学意义。随杨梅素浓度增加，线粒体途径的促凋亡因子BAX蛋白表达量增加，而抗凋亡因子BCL-2蛋白表达量降低。结论杨梅素能够诱导HepG2细胞凋亡，可能具有潜在的抗肝癌活性；线粒体途径在此过程中起重要作用。
목적：탐토양매소대인간암세포계 HepG2조망적영향급기궤제。방법이불동농도적양매소부육HepG2세포，재불동시간분별채용도치현미경관찰세포형태학변화；채용새서람（MTT）법검측세포존활솔；채용유산탈경매（LDH）활력정량측정시제합측정세포상청액LDH활성；채용류식세포술검측세포조망솔；채용단백질인적법검측세포조망도경관건단백적표체。결과양매소대HepG2세포적조망유도작용정현제량화시간의뢰성。양매소작용우HepG2세포，수양매소농도증가，세포조망솔증가。여정상대조조상비，100μmol/L양매소작용우HepG2세포24 h후，세포존활솔명현강저[（100.02±5.97）%vs.（71.60±3.75）%，P=0.006]；조、만기세포조망솔명현승고[（10.19±2.61）%vs.（2.52±2.05）%，P=0.003；（11.71±3.34）%vs.（3.69±1.13）%，P=0.004]，차이균유통계학의의。수양매소농도증가，선립체도경적촉조망인자BAX단백표체량증가，이항조망인자BCL-2단백표체량강저。결론양매소능구유도HepG2세포조망，가능구유잠재적항간암활성；선립체도경재차과정중기중요작용。
Objective To study the effect of myricetin on HepG2 apoptosis. Methods HepG2 cell was incubated with different concentrations of myricetin. Cell viability was measured by MTT method. Apoptosis was measured by flow cytometry. The expressions of the key protein of apoptosis were detected by western blot. Results The reduction of cell viability was more significant with the increase of myricetin concentration. In the 100μmol/L myricetin for 24h group,the cell viability was lower than the control group[(71.6±3.75)%vs. (100.02±5.97)%,P=0.006], the early and late apoptosis rate were higher than the control group[(10.19±2.61)%vs. (2.52±2.05)%,P=0.003;(11.71±3.34)%vs. (3.69±1.13)%, P=0.004]. The expression of pro-apoptotic factor BAX protein was increased, while the anti-apoptotic factor BCL-2 pro-tein expression was reduced. Conclusion Myricetin could induce apoptosis of HepG2 cell through mitochondrial pathway, indicating that myricetin might inhibit hepatocellular carcinoma progression.