Ha Min-Wen, Ma Rui, Shun Li-Ping, Gong Yue-Hua, Yuan Yuan
Cancer Institute of the First Affiliated Hospital of China Medical University, 155 Northern Nanjing Street, Heping District, Shenyang 110001, Liaoning Province, China.
World J Gastroenterol. 2005 Sep 21;11(35):5433-7. doi: 10.3748/wjg.v11.i35.5433.
To determine the effect of allitridi on cell cycle of human gastric cancer (HGC) cell lines MGC803 and SGC7901 and its possible mechanism.
Trypan blue dye exclusion was used to evaluate the proliferation, inhibition of cells and damages of these cells were detected with electron microscope. Flow cytometry and cell mitotic index were used to analyze the change of cell cycle, immunohistochemistry, and RT-PCR was used to examine expression of the p21(WAF1) gene.
MGC803 cell growth was inhibited by allitridi with 24 h IC50 being 6.4 microg/mL. SGC7901 cell growth was also inhibited by allitridi with 24 h IC50 being 7.3 microg/mL. After being treated with allitridi at the concentration of 12 microg/mL for 24 h, cells were found to have direct cytotoxic effects, including broken cellular membrane, swollen and vesiculated mitochondria and rough endoplasmic reticula, and mass lipid droplet. When cells were treated with allitridi at the concentration of 3, 6, and 9 microg/mL for 24 h, the percentage of G0/G1 phase cells was decreased and that of G2/M phase cells was significantly increased (P = 0.002) compared with those in the group. When cells were treated with allitridi at the concentration of 6 microg/mL, cell mitotic index was much higher (P = 0.003) than that of control group, indicating that allitridi could cause gastric cancer cell arrest in M phase. Besides, the expression levels of p21(WAF1) gene of MGC803 cells and p21(WAF1) gene of SGC7901 cells were remarkably upregulated after treatment.
Allitridi can cause gastric cancer cell arrest in M phase, and this may be one of the mechanisms for inhibiting cell proliferation. Effect of allitridi on cells in M phase may be associated with the upregulation of p21(WAF1) genes. This study provides experimental data for clinical use of allitridi in the treatment of gastric carcinoma.
探讨大蒜素对人胃癌细胞系MGC803和SGC7901细胞周期的影响及其可能机制。
采用台盼蓝拒染法评价细胞增殖情况，用电子显微镜检测细胞损伤情况。采用流式细胞术和细胞有丝分裂指数分析细胞周期变化，用免疫组织化学和逆转录-聚合酶链反应（RT-PCR）检测p21（WAF1）基因表达。
大蒜素可抑制MGC803细胞生长，24小时半数抑制浓度（IC50）为6.4微克/毫升。大蒜素也可抑制SGC7901细胞生长，24小时IC50为7.3微克/毫升。用12微克/毫升大蒜素处理细胞24小时后，发现细胞有直接细胞毒性作用，包括细胞膜破裂、线粒体肿胀和空泡化、粗面内质网扩张以及大量脂滴。当用3、6和9微克/毫升大蒜素处理细胞24小时时，与对照组相比，G0/G1期细胞百分比降低，G2/M期细胞百分比显著增加（P = 0.002）。当用6微克/毫升大蒜素处理细胞时，细胞有丝分裂指数比对照组高得多（P = 0.003），表明大蒜素可使胃癌细胞停滞于M期。此外，处理后MGC803细胞和SGC7901细胞的p21（WAF1）基因表达水平均显著上调。
大蒜素可使胃癌细胞停滞于M期，这可能是其抑制细胞增殖的机制之一。大蒜素对M期细胞的作用可能与p21（WAF1）基因上调有关。本研究为大蒜素临床治疗胃癌提供了实验依据。
