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作 者:江莲[1] 李雪青[2] 赵孝先[1] 刘翠萍[1] 李梅[1] 曲凡[1] 金江[1]
机构地区:[1]河北医科大学第四医院儿科,河北石家庄050011 [2]天津武警医学院附属医院儿科,天津300011
出 处:《临床儿科杂志》2008年第11期940-945,共6页Journal of Clinical Pediatrics
摘 要:目的探讨选择性COX-2抑制剂塞来昔布(celecoxib)对恶性淋巴瘤细胞的作用及其抗肿瘤的非COX-2依赖性途径之可能机制。方法体外培养人Burkitt淋巴瘤Raji细胞,用不同浓度的塞来昔布进行干预。应用MTT比色法检测Raji细胞生长情况;流式细胞术分析塞来昔布对Raji细胞周期的影响并检测细胞凋亡及Survivin蛋白在细胞中的表达情况;应用RT-PCR法检测Raji细胞中Survivin mRNA的表达水平。结果塞来昔布对Raji细胞生长具有抑制作用,且在12.5~150μmol/L范围内呈时间、剂量依赖性;流式细胞术检测出典型的凋亡峰,凋亡率(9.20±0.19)%~(44.63±1.34)%;塞来昔布使Raji细胞G0/G1期细胞数增多,S和G2/M期细胞数减少,凋亡率和细胞周期分布呈量效依赖关系;塞来昔布下调Raji细胞中Survivin蛋白和Survivin mRNA的表达。结论塞来昔布抑制Raji细胞增殖、诱导其凋亡可能与阻滞细胞周期和下调Survivin表达有关,这可能是其抗肿瘤的非COX-2依赖性途径之机制。Objectives To investigate the effect of celecoxib (a selective COX-2 inhibitor) on proliferation, apoptosis, cell cycle distribution and snrvivin expression in human malignant lymphoma cell line Raji and the possible antitumor mechanism in COX-2 independent pathway of eeleeoxih. Methods Human Burkitt's lymphoma cells Raji were cultivated in vitro and treated with various concentrations of eelecoxib. Cell inhibitive rate was investigated by MTT assay. Apoptosis rate, cell cycle distribution and expression of survivin protein in Raji cells were detected by flow cytometry (FCM). Expression of survivin mR NA in Raji cells was detected by RT-PCR. Results The growth of Raji cells was inhibited by celecoxib in a concentration and time dependent manners within the range of 12.5 - 150 μmol/L. The typical apoptosis peak was detected by FCM, and the apoptotic rate was between (9.20 ± 0.19)% and (44.63 ±1.34)%. The cell percentage in G0/G1 phase increased, whereas the cell percentage in S and G2/M phase decreased, the apoptotie rate and cell cycle distribution were in concentration dependent manners, celecoxib downregulated the expression of survivin protein and survivin mRNA in Raji cells. Conclusions The inhibitory eft)ct of celecoxib on cell Raji and its ability to induce cell apoplosis may relate to its blocking of cell cycle progress and downregulating the expression of survivin, which may be a possible antitumor mechanism of celecoxih in COX-2 independent pathway.
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