中国生化药物杂志
中國生化藥物雜誌
중국생화약물잡지
Chinese Journal of Biochemical Pharmaceutics
2015年
10期
11-14
,共4页
赵成亮%宋有鑫%赵龙%张四喜%李连泰
趙成亮%宋有鑫%趙龍%張四喜%李連泰
조성량%송유흠%조룡%장사희%리련태
Zn(PMFPCl)2%HepG2细胞%增殖%细胞周期%凋亡相关蛋白
Zn(PMFPCl)2%HepG2細胞%增殖%細胞週期%凋亡相關蛋白
Zn(PMFPCl)2%HepG2세포%증식%세포주기%조망상관단백
Zn(PMFPCl) 2%HepG2 cells%proliferation%cell cycle%apoptosis-regulated proteins
目的 探究Zn(PMFPCl)2 对肝癌HepG2细胞的抑制作用及其机制.方法 HepG2细胞分组为对照组及实验组(10、30、70μmol/L).MTT法检测Zn(PMFPCl) 2 对肝癌HepG2细胞增殖的影响,流式细胞仪检测细胞凋亡及细胞周期,倒置显微镜下观察Zn(PMFPCl) 2 作用后肿瘤细胞的形态学变化,Western blot检测凋亡蛋白p53、p21、caspase-3、bax、bcl-2的表达情况.结果 各实验组(10、30、70μmol/L)在24、48、72 h对细胞的抑制率均显著高于对照组(P<0.05).当Zn(PMFPCl)2 浓度70μmol/L,作用72 h时细胞的抑制率最高,达63.29%.各实验组在48 h时的细胞凋亡率显著高于对照组(P<0.05).Zn(PMFPCl)2 使细胞的生长停滞在G1期,阻碍细胞增殖.当Zn(PMFPCl) 2 作用细胞后贴壁细胞数量减少,细胞皱缩,细胞膜出现突起,细胞变圆、变亮.Western blot法检测p53、p21、caspase-3、bax随配合物浓度的增加而增加,而bcl-2随之减少(P<0.05).结论 Zn(PMFPCl)2 对肝癌HepG2细胞具有抑制增殖及促进凋亡的作用,其机制与促进p53、p21、caspase-3、bax表达而降低bcl-2表达有关.
目的 探究Zn(PMFPCl)2 對肝癌HepG2細胞的抑製作用及其機製.方法 HepG2細胞分組為對照組及實驗組(10、30、70μmol/L).MTT法檢測Zn(PMFPCl) 2 對肝癌HepG2細胞增殖的影響,流式細胞儀檢測細胞凋亡及細胞週期,倒置顯微鏡下觀察Zn(PMFPCl) 2 作用後腫瘤細胞的形態學變化,Western blot檢測凋亡蛋白p53、p21、caspase-3、bax、bcl-2的錶達情況.結果 各實驗組(10、30、70μmol/L)在24、48、72 h對細胞的抑製率均顯著高于對照組(P<0.05).噹Zn(PMFPCl)2 濃度70μmol/L,作用72 h時細胞的抑製率最高,達63.29%.各實驗組在48 h時的細胞凋亡率顯著高于對照組(P<0.05).Zn(PMFPCl)2 使細胞的生長停滯在G1期,阻礙細胞增殖.噹Zn(PMFPCl) 2 作用細胞後貼壁細胞數量減少,細胞皺縮,細胞膜齣現突起,細胞變圓、變亮.Western blot法檢測p53、p21、caspase-3、bax隨配閤物濃度的增加而增加,而bcl-2隨之減少(P<0.05).結論 Zn(PMFPCl)2 對肝癌HepG2細胞具有抑製增殖及促進凋亡的作用,其機製與促進p53、p21、caspase-3、bax錶達而降低bcl-2錶達有關.
목적 탐구Zn(PMFPCl)2 대간암HepG2세포적억제작용급기궤제.방법 HepG2세포분조위대조조급실험조(10、30、70μmol/L).MTT법검측Zn(PMFPCl) 2 대간암HepG2세포증식적영향,류식세포의검측세포조망급세포주기,도치현미경하관찰Zn(PMFPCl) 2 작용후종류세포적형태학변화,Western blot검측조망단백p53、p21、caspase-3、bax、bcl-2적표체정황.결과 각실험조(10、30、70μmol/L)재24、48、72 h대세포적억제솔균현저고우대조조(P<0.05).당Zn(PMFPCl)2 농도70μmol/L,작용72 h시세포적억제솔최고,체63.29%.각실험조재48 h시적세포조망솔현저고우대조조(P<0.05).Zn(PMFPCl)2 사세포적생장정체재G1기,조애세포증식.당Zn(PMFPCl) 2 작용세포후첩벽세포수량감소,세포추축,세포막출현돌기,세포변원、변량.Western blot법검측p53、p21、caspase-3、bax수배합물농도적증가이증가,이bcl-2수지감소(P<0.05).결론 Zn(PMFPCl)2 대간암HepG2세포구유억제증식급촉진조망적작용,기궤제여촉진p53、p21、caspase-3、bax표체이강저bcl-2표체유관.
Objective To explore the inhibition of Zn(PMFPCl) 2 on HepG2 cells and its mechanism.Methods The HepG2 cells were divided into control group and experimental group of 10, 30 and 70 μmol/L.The cell proliferation was detected by MTT assay, cell apoptosis and cell cycle was analysed by flow cytometry, cellular morphological change was observed with inverted microscope and the expressions of apoptosis-regulated proteins of p53, p21, caspase-3, bax and bcl-2 in HepG2 cells were detected by Western blot.Results The inhibitory rates of experimental groups (10, 30, 70μmol/L) at 24, 48 and 72h were significantly higher than those of control group (P<0.05), and the highest one was 63.29% of 70 μmol/L Zn (PMFPCl)2at 72 h.The apoptosis rates of each experimental group at 48h was significantly higher than that of control group (P<0.05).The cells were induced a remarkable G1 arrest by Zn(PMFPCl) 2 which could inhibit proliferation.The number of adherent cells reduced and cells shrank, convex on cytomembrane surface appeared and the cells changed to round and were brighter.Western blot results showed that the protein levels of p53, p21, caspase-3 and bax increased and bcl-2 decreased with the Zn(PMFPCl)2concentration increasing (P<0.05).Conclusion Zn(PMFPCl)2 could inhibit the proliferation and promote apoptosis of HepG2 cells whose mechanisms are promotation of p53, p21, caspase-3 and bax expressions and inhibition of bcl-2 expression.