Song Guanbin, Luo Qing, Qin Jian, Wang Lu, Shi Yisong, Sun Caixin
College of Bioengineering, Chongqing University, Key Laboratory of Biomechanics and Tissue Engineering, State Ministry of Education, Chongqing 400044, PR China.
Colloids Surf B Biointerfaces. 2006 Mar 1;48(1):1-5. doi: 10.1016/j.colsurfb.2005.12.012. Epub 2006 Feb 3.
Oxymatrine, a natural quinolizidine alkaloid, has been known having cytotoxic and chemopreventive effects on various cancer cells. To investigate the possible mechanism of oxymatrine's role on cancer cells, in the present study, we examined further the effects of oxymatrine on the growth, proliferation, apoptosis and expression of bcl-2 and p53 gene in human hepatoma SMMC-7721 cells in vitro. Our results show that oxymatrine notably inhibits the growth and proliferation of SMMC-7721 cells and it present a dose-dependence and time-dependence manner within definite reacting dose and time. Oxymatrine block SMMC-7721 cells in G2/M and S phase; prevent cells entering into G0/G1 phase. It results in an obvious accumulation of G2/M and S phase cells while decrease of G0/G1 phase cells. Oxymatrine induce apoptosis of SMMC-7721 cells and apoptotic rate amount to about 60% after treatment with 1.0 mg/ml oxymatrine for 48 h. We also find that oxymatrine down-regulate expression of bcl-2 gene while up-regulate expression of p53 gene. These results demonstrate that oxymatrine inhibit the proliferation and induce apoptosis of human hepatoma SMMC-7721 cells, and suggest that this effect was mediated probably by a significant cell cycle blockage in G2/M and S phase, down-regulation of bcl-2 and up-regulation of p53.
氧化苦参碱是一种天然的喹诺里西啶生物碱，已知对多种癌细胞具有细胞毒性和化学预防作用。为了研究氧化苦参碱对癌细胞作用的可能机制，在本研究中，我们进一步检测了氧化苦参碱对人肝癌SMMC-7721细胞体外生长、增殖、凋亡以及bcl-2和p53基因表达的影响。我们的结果表明，氧化苦参碱显著抑制SMMC-7721细胞的生长和增殖，并且在一定的反应剂量和时间范围内呈现剂量依赖性和时间依赖性。氧化苦参碱将SMMC-7721细胞阻滞在G2/M期和S期；阻止细胞进入G0/G1期。这导致G2/M期和S期细胞明显积聚，而G0/G1期细胞减少。氧化苦参碱诱导SMMC-7721细胞凋亡，用1.0mg/ml氧化苦参碱处理48小时后凋亡率约为60%。我们还发现氧化苦参碱下调bcl-2基因的表达，同时上调p53基因的表达。这些结果表明，氧化苦参碱抑制人肝癌SMMC-7721细胞的增殖并诱导其凋亡，提示这种作用可能是通过G2/M期和S期显著的细胞周期阻滞、bcl-2的下调和p53的上调介导的。
