论文部分内容阅读
目的探讨不同CO2压强及时程对MKN-28细胞黏附侵袭能力的影响。方法利用密封箱建立体外气腹模型,选用胃癌细胞株MKN-28,分别在9mmHg(1mmHg=0.133kPa)和15mmHg压强下以及常规条件下暴露2h和4h后,用CytoMatrixTM细胞黏附试剂盒检测细胞黏附能力,流式细胞技术(FACScan)检测表达E-钙黏蛋白(E-cadherin)和细胞间黏附分子(Intercellular adhesion molecule-1,ICAM-1)的细胞百分数。另将处理后的MKN-28细胞注入裸鼠腹腔(2×106个细胞/只),每组10只。4周后每组取5只处死,记录腹腔成瘤情况,剩余裸鼠观察生存时间。结果MKN-28细胞株经不同压强与不同时程的CO2处理后,胃癌细胞MKIN-28黏附能力,表达E-cadherin和ICAM-1的细胞百分数MKN-28的腹腔内转移个数,生存天数,裸鼠腹腔种植成瘤数和生存时间各组间均差异均无统计学意义(P>0.05)。结论在不高于15mmHg压强,且不超过4h情况下,不同CO2压强及不同时程对MKN-28细胞株的黏附侵袭能力并无显著影响,亦不增加肿瘤的转移几率。
Objective To investigate the effects of different CO2 pressures and time courses on the adhesion and invasion of MKN-28 cells. Methods The pneumoperitoneum model was established by using a sealed box. The gastric cancer cell line MKN-28 was selected and the cells were stained with CytoMatrixTM Cell Adhesion Kit at 9mmHg (1mmHg = 0.133kPa) and 15mmHg for 2h and 4h, respectively. The percentage of cells expressing E-cadherin and Intercellular adhesion molecule-1 (ICAM-1) was detected by flow cytometry (FACScan). In addition, the treated MKN-28 cells were injected into the peritoneal cavity of nude mice (2 × 10 6 cells / mouse), 10 in each group. After 4 weeks, 5 rats in each group were sacrificed and the celiac tumor formation was recorded. The remaining nude mice were observed for survival time. Results After MKN-28 cells were treated with different pressures and time courses of CO2, MKN-28 cell adhesion ability, the number of cells expressing E-cadherin and ICAM-1 MKN-28 intraperitoneal metastasis, survival days, There was no significant difference between the two groups in tumor formation and survival time (P> 0.05). Conclusion Under the condition of no higher than 15mmHg pressure and no longer than 4h, different CO2 pressures and different time courses have no significant effect on the adhesion and invasion ability of MKN-28 cell lines, and do not increase the probability of tumor metastasis.