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目的揭示COX-2选择性抑制剂NS398对肾癌细胞的增殖和凋亡作用的影响,及其可能的作用机制。方法采用标准的细胞培养方法对人肾癌786-0细胞进行培养,将NS398分别以不同浓度剂量加入细胞中作用24及48h后,应用流式细胞仪检测凋亡,应用RT-PCR和Western blotting检测COX-2和Bcl-2表达的改变。结果NS398对肾癌786-0细胞具有较强的抑制作用,且这种抑制作用随浓度和时间的增加而增大,呈浓度依赖关系(P<0.05);RT-PCR和Western Blot结果表明,不同浓度NS398作用下的肾癌786-0细胞中,COX-2和Bcl-2的表达明显减弱,且呈剂量梯度下降。NS398作用于肾癌786-0细胞24h后,在细胞周期G0/G1期前出现明显的亚二倍体凋亡峰,随着浓度的升高,凋亡峰亦越来越高(P<0.05)。结论肾癌786-0细胞中存在着COX-2的过表达;选择性COX-2抑制剂NS398通过诱导凋亡来抑制肾癌786-0细胞的增殖,其机制可能是通过抑制COX-2的表达及下调Bcl-2来完成的。
Objective To reveal the effect of COX-2 selective inhibitor NS398 on the proliferation and apoptosis of renal cell carcinoma and its possible mechanism. Methods Human renal cell carcinoma 786-0 cells were cultured by standard cell culture method. After NS398 cells were treated with different concentrations for 24 and 48 hours respectively, apoptosis was detected by flow cytometry. The expression of apoptosis was detected by RT-PCR and Western blotting The changes of COX-2 and Bcl-2 expression were detected. Results NS398 had a strong inhibitory effect on 786-0 human renal cell carcinoma cell line, and this inhibitory effect increased with concentration and time increasing in a concentration-dependent manner (P <0.05). The results of RT-PCR and Western Blot showed that, The expression of COX-2 and Bcl-2 in renal cancer 786-0 cells with different concentrations of NS398 significantly decreased, and the dose gradient decreased. After treated with NS398 for 24 h, the apoptotic peak of sub-diploid cells appeared at the G0 / G1 phase of cell cycle, and the peak of apoptosis increased with increasing concentration of NS398 (P <0.05 ). Conclusion The overexpression of COX-2 exists in 786-0 cell line of renal cell carcinoma. NS398, a selective COX-2 inhibitor, inhibits the proliferation of 786-0 cell line by inducing apoptosis. The mechanism may be that COX-2 Expression and down-regulation of Bcl-2.