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目的旨在了解环氧合酶-2(cyc looxygenase-2,COX-2)抑制剂美洛昔康对胃癌细胞的长期作用能否导致胃癌细胞对其产生耐药性。方法采用浓度递增法结合大剂量冲击法,美洛昔康长期作用于胃癌SGC7901细胞,时间达6个月,尝试诱导胃癌美洛昔康耐药株,命名为SGC7901/M,并用MTT法测定药物敏感性,光镜、电镜观察细胞形态学改变,活细胞计数法和克隆形成技术了解其生物学特性。结果药物敏感分析显示,胃癌细胞经过美洛昔康长期作用,对美洛昔康并没有出现抗性,其IC50与亲代细胞比较差异无统计学意义(P>0.05),分别为4.6×10-4±2.23×10-4mol.L-1,3.54×10-4±2.34×10-4mol.L-1。SGC7901/M细胞对美洛昔康的耐药指数约为1.3。SGC7901/M细胞与亲代细胞形态学比较,光镜及电镜均未显示差异,两种细胞在经1×10-3mol.L-1美洛昔康作用24 h后,均表现出细胞受到明显损伤和凋亡的形态。无论从生长曲线上还是克隆形成率上都显示SGC7901/M细胞与亲代细胞的生长特性无差异。结论美洛昔康可抑制胃癌细胞生长,长期用药不诱导胃癌细胞产生耐药性。
The purpose is to understand whether long-term effects of meloxicam, a cyclooxygenase-2 inhibitor (COX-2) inhibitor, on gastric cancer cells can cause gastric cancer cells to develop resistance to them. Methods The concentration-increasing method combined with high-dose impact method, meloxican long-term effect on gastric cancer SGC7901 cells for 6 months, trying to induce meloxicam gastric cancer, named SGC7901 / M, and MTT assay of drugs Sensitivity, light microscopy, electron microscopy morphological changes of cells, viable cell counting method and clone formation technology to understand its biological characteristics. Results The results of drug sensitivity analysis showed that the long-term effect of meloxicam on gastric cancer cells showed no resistance to meloxicam. The IC50 of the cells was no significant difference from that of the parental cells (4.6 × 10- 4 ± 2.23 × 10 -4 mol.L-1, 3.54 × 10 -4 ± 2.34 × 10 -4 mol·L -1. The resistance index of meloxicam in SGC7901 / M cells was about 1.3. SGC7901 / M cells compared with the parental cell morphology, light and electron microscopy showed no difference between the two cells in the 1 × 10-3mol.L-1 meloxicam effect of 24 h after the cells were significantly damaged And the morphology of apoptosis. There was no difference in growth characteristics between SGC7901 / M cells and parental cells in both growth curve and clone formation rate. Conclusion Meloxicam can inhibit the growth of gastric cancer cells, long-term drug does not induce gastric cancer cells produce drug resistance.