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舒林酸抗胃癌细胞体外生长的实验研究
引用本文:Yu DH,Zhou L,Wang P,Wang QZ,Cheng ZN. 舒林酸抗胃癌细胞体外生长的实验研究[J]. 中华肿瘤杂志, 2006, 28(7): 498-502
作者姓名:Yu DH  Zhou L  Wang P  Wang QZ  Cheng ZN
作者单位:1. 233003,蚌埠医学院病理学教研室安徽省感染与免疫重点实验室
2. 蚌埠医学院附属医院消化科
基金项目:安徽省教育厅自然科学研究项目(2003kj257);蚌埠市科技三项费用项目(2003-10)
摘    要:
目的观察舒林酸对胃癌BGC-823细胞增殖、凋亡的影响,探讨其作用机制。方法将不同浓度的舒林酸体外作用于人胃癌BGC-823细胞,采用倒置显微镜观察BGC-823细胞形态改变,四甲基偶氮唑蓝(MTT)比色法检测胃癌细胞增殖,流式细胞仪检测胃癌细胞周期分布及凋亡,透射电镜观察凋亡,免疫组化检测ki-67、bcl-2及环氧合酶-2(COX-2)蛋白的表达。结果舒林酸作用后,细胞伪足回缩,变小、变圆,排列松散或聚集成团,出现悬浮现象,瘤巨细胞减少或不见瘤巨细胞。舒林酸可抑制BGC-823细胞增殖,使G0/G1期细胞比例增高,S期细胞比例降低。1.2mmol/L舒林酸作用48h,G0/G1期细胞增至93.8%,S期细胞比例降至3.4%。舒林酸作用后,细胞凋亡率显著上升,1.2mmol/L舒林酸作用48h,细胞凋亡率升至54.9%,而ki-67、bcl-2及COX-2蛋白表达阳性率显著降低;透射电镜可观察到细胞凋亡的形态特征及凋亡小体。上述作用均呈时间和剂量依赖性。结论舒林酸可抑制胃癌BGC--823细胞体外生长,其机制涉及影响细胞周期分布、诱导细胞凋亡及抑制ki-67、bcl-2及COX-2蛋白的表达。

关 键 词:舒林酸 胃癌细胞 增殖 凋亡 环氧合酶-2
收稿时间:2005-07-06
修稿时间:2005-07-06

Inhibition of gastric cancer cells growth in vitro by sulindac
Yu Dong-Hong,Zhou Lei,Wang Ping,Wang Qi-Zhi,Cheng Ze-Nong. Inhibition of gastric cancer cells growth in vitro by sulindac[J]. Chinese Journal of Oncology, 2006, 28(7): 498-502
Authors:Yu Dong-Hong  Zhou Lei  Wang Ping  Wang Qi-Zhi  Cheng Ze-Nong
Affiliation:Department of Pathology, Bengbu Medical College, Bengbu 233003, China
Abstract:
Objective To investigate the effect of sulindac on proliferation and apoptosis of human gastric cancer BGC-823 cells and its antineoplastic mechanisms. Methods Human gastric cancer BGC-823 cells were incubated with sulindac at various concentrations and for different times. Morphological changes of BGC-823 cells were observed under an inversion microscope. MTT colorimetric assay was used to examine the effect of sulindac on the proliferation of BGC-823 cells. Flow cytometry was used to determine the cell cycle distribution and apoptosis. Transmission electron microscopy was performed to examine cell apoptosis morphology. Immunohistochemical staining was used to detect the expressions of COX-2, bcl-2 and ki-67 in the cells. Results sulindac induced morphologic alterations in BGC-823 cells, inhibited cell proliferation, increased the proportion of cells in G0/G1 phase and decreased the proportion of cells in S phase, induced apoptosis of BGC-823 cells, and decreased expressions of COX-2, bcl-2, ki-67 in the cells. All the effects were in a time- and dose-dependent manner (P < 0. 05). Some characteristic morphologic features of apoptosis were revealed by transmission electron microscopy. Conclusion sulindac may inhibit the growth of gastric cancer BGC-823 cells in vitro and the anti-tumor mechanism may be related to changes in cell cycle distribution, induction of apoptosis and inhibition of expression of COX-2, bcl-2, and ki-67.
Keywords:Sulindac    Gastric cancer cells   Proliferation    Apoptosis    Cyclooxygenase-2
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