CAJ | 학술논문

目的：观察明矾对HepG2、SMMC-7721肝癌细胞增殖的影响，并探讨其可能机制。方法选取HepG2、SMMC-7721肝癌细胞株，分别设置实验组及对照组（ HepG2细胞设为实验1组及对照1组，SMMC-7721细胞设为实验2组及对照2组），实验组加入不同剂量明矾，对照组加入等体积的DMEM培养基，台盼蓝实验做细胞生长曲线；流式细胞分析技术检测各组细胞周期、凋亡变化；RT-PCR、ELISA法分别检测细胞内转化生长因子β1（ TGF-β1）、p21、Cyclin E mRNA及蛋白表达。结果100μg／mL的明矾对HepG2细胞株在第3、4、5、6天的抑制率分别为23．2％、53．7％、68．6％、97．3％，100μg／mL的明矾对SMMC-7721细胞株在第3、4、5、6天的抑制率分别为14．1％、28．3％、47．2％、81．9％。 HepG2细胞：实验1组及对照1组G0／G1期细胞比例分别为73．15％、59．75％，两组比较， P＜0．05；SMMC-7721细胞：实验2组及对照2组G0／G1期细胞比例分别为76．66％、44．11％，两组比较，P＜0．05。HepG2细胞：实验1组及对照1组细胞凋亡率分别为22．53％、5．20％，两组比较，P＜0．05；SMMC-7721细胞：实验2组及对照2组细胞凋亡率分别为17．63％、4．80％，两组比较，P＜0．05。与其相对应的对照组比较，实验组TGF-β1 mRNA及蛋白表达升高，p21 mRNA及蛋白表达升高，Cyclin E mRNA及蛋白表达降低（P＜0．05或0．01）。结论明矾能够抑制肝癌细胞增殖，使肝癌细胞阻滞于G1期，并促进其凋亡，其机制可能与促进TGF-β1、p21表达及下调Cyclin E表达有关。
목적：관찰명반대HepG2、SMMC-7721간암세포증식적영향，병탐토기가능궤제。방법선취HepG2、SMMC-7721간암세포주，분별설치실험조급대조조（ HepG2세포설위실험1조급대조1조，SMMC-7721세포설위실험2조급대조2조），실험조가입불동제량명반，대조조가입등체적적DMEM배양기，태반람실험주세포생장곡선；류식세포분석기술검측각조세포주기、조망변화；RT-PCR、ELISA법분별검측세포내전화생장인자β1（ TGF-β1）、p21、Cyclin E mRNA급단백표체。결과100μg／mL적명반대HepG2세포주재제3、4、5、6천적억제솔분별위23．2％、53．7％、68．6％、97．3％，100μg／mL적명반대SMMC-7721세포주재제3、4、5、6천적억제솔분별위14．1％、28．3％、47．2％、81．9％。 HepG2세포：실험1조급대조1조G0／G1기세포비례분별위73．15％、59．75％，량조비교， P＜0．05；SMMC-7721세포：실험2조급대조2조G0／G1기세포비례분별위76．66％、44．11％，량조비교，P＜0．05。HepG2세포：실험1조급대조1조세포조망솔분별위22．53％、5．20％，량조비교，P＜0．05；SMMC-7721세포：실험2조급대조2조세포조망솔분별위17．63％、4．80％，량조비교，P＜0．05。여기상대응적대조조비교，실험조TGF-β1 mRNA급단백표체승고，p21 mRNA급단백표체승고，Cyclin E mRNA급단백표체강저（P＜0．05혹0．01）。결론명반능구억제간암세포증식，사간암세포조체우G1기，병촉진기조망，기궤제가능여촉진TGF-β1、p21표체급하조Cyclin E표체유관。
Objective To observe the influence of alum on the liver carcinoma cells HepG2 and SMMC-7721, and to investigate its possible mechanism.Methods HepG2, SMMC-7721 cell lines were selected and we set the experimental group and control group ( HepG2 cells were divided into the experimental group 1 and the control group 1, SMMC-7721 cells were divided into the experimental group 2 and the control group 2) .Cells in the experimental group were added with different dosages of alum and the control group with the same volume of DMEM medium.Trypan blue tests were conducted to analyze cell growth curve;the cell cycle and apoptosis were detected by flow cytometry;and RT-PCR, ELISA were used to detect the mRNA and protein expression of transforming growth factor-β1 ( TGF-β1 ) , p21 and Cyclin E.Results For HepG2 cell line, the inhibition rates of 100 μg/mL alum at day 3, 4, 5 and 6 were 23.2%, 53.7%, 68.6% and 97.3%, respectively.For SMMC-7721 cell line, the inhibition rates of 100 μg/mL alum at day 3, 4, 5 and 6 were 14.1%, 28.3%, 47.2%and 81.9%.HepG2 cells:the cell proportion in the G0/G1 phase of the experimental group 1 and control group 1 was 73.15%and 59.75%, respectively (P<0.05).SMMC-7721 cells: the cell proportion in the G0/G1 phase of the experimental group 2 and control group 2 was 76.66%and 44.11%respectively (P<0.05).HepG2 cells:the apoptosis rates of the experimental group 1 and control group 1 were 22.53% and 5.2%, respectively ( P<0.05).SMMC-7721 cells:the apoptosis rates of the experimental group 2 and control group 2 were 17.63% and 4.8%, respectively (P<0.05).Compared with its corresponding control groups, the mRNA and protein expression of TGF-β1 was increased, p21 mRNA and protein expression was increased and Cyclin E mRNA and protein expression was decreased in the experimental groups (P<0.05 or P<0.01).Conclusion Alum may inhibit the proliferation of liver cancer cells, ar-rest cells at G1 phase and promote their apoptosis, which are associated with the increased TGF-β1 and p21 expression and the down-regulation of Cyclin E expression.