论文部分内容阅读
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。1．2 mmoL／L舒林酸作用48 h,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,1．2 mmoL／L舒林酸作用48 h,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。
Objective To observe the effect of sulindac on the proliferation and apoptosis of gastric cancer BGC-823 cells, and to explore its mechanism of action. Methods Different concentrations of sulindac were used to treat human gastric cancer BGC-823 cells in vitro. The morphology of BGC-823 cells was observed by inverted microscope. The proliferation of gastric cancer cells was detected by MTT assay. Flow cytometry The cell cycle distribution and apoptosis of gastric cancer cells were detected. The apoptosis was observed by transmission electron microscope. The expression of ki-67, bcl-2 and cyclooxygenase-2 (COX-2) protein was detected by immunohistochemistry. RESULTS: After sulindac treatment, the pseudopods retracted, became smaller and rounder, and arranged loosely or clustered together. Suspension occurred, and the giant cells of the tumor were reduced or tumor giant cells were not seen. Sulindac inhibited the proliferation of BGC-823 cells, increased the proportion of G0/G1 phase cells, and decreased the proportion of S phase cells. When treated with 1.2 mmoL/L sulindac for 48 h, the cells in G0/G1 phase increased to 93.8%, and the proportion of cells in S phase decreased to 3.4%. After sulindac treatment, the apoptosis rate increased significantly. After 1.2 mmoL/L sulindac treatment for 48 h, the apoptosis rate increased to 54.9%, while the ki-67, bcl-2, and COX-2 proteins. The positive rate of expression was significantly reduced; morphological features of apoptotic cells and apoptotic bodies were observed by transmission electron microscopy. The above effects are time and dose dependent. Conclusion Sulindac can inhibit the growth of gastric cancer BGC-823 cells in vitro. Its mechanism involves affecting cell cycle distribution, inducing apoptosis and inhibiting the expression of ki-67, bcl-2 and COX-2 proteins.