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机构地区:[1]哈尔滨医科大学第一临床医学院普外科,150001 [2]黑龙江省佳木斯市中心医院,154000 [3]浙江省玉环县第二人民医院外科,317600
出 处:《重庆医学》2008年第6期635-636,662,共3页Chongqing medicine
摘 要:目的观察尼美舒利对脱氧胆酸(DCA)诱导的人结肠癌HT-29细胞增殖的抑制作用,探讨其可能的机制。方法200μmol/L DCA加到HT-29细胞培养液中,同时给予不同浓度尼美舒利(50、75、100μmol/L),采用MTT法测定细胞增殖;RT-PCR法检测环氧合酶-2(COX-2)mRNA,免疫组化染色法检测细胞COX-2表达,放免法检测前列腺素E2(PGE2)含量。结果DCA作用HT-29细胞6h,COX-2蛋白表达阳性率较对照组明显升高〔(64.2±6.2)%或(7.1±1.9)%〕,PGE2合成增加〔(23.9±1.3)ng/L或(10.5±0.9)ng/L〕,尼美舒利对DCA诱导的HT-29细胞作用6h可抑制细胞增殖,并可抑制DCA诱导的COX-2mRNA表达,抑制PGE2合成,上述作用均呈浓度-时间依赖性。结论尼美舒利可抑制DCA诱导的HT-29人结肠癌细胞增殖,抑制COX-2 mRNA表达和蛋白表达及PGE2合成,这可能是尼美舒利抑制HT-29细胞增殖的机制之一。Objective To investigate the effect of nimesulide on inhibiting HT-29 human colon cancer cell proliferation induced by deoxycholic acid (DCA). Methods The nimesulide with concentration of 50,75 or 100μmol/L were added into the HT-29 human colon cancer cell culture media containing 200μmol/L DCA. The effects of Nimesulide on cell proliferation were studied by the method of MTT. RT-PCR was applied to measure the expression of cyclooxygenase 2 (COX-2) mRNA. Cellular immunochemical stain was applied to label COX-2 protein expression. Concentration of prostaglandin E2 (PGE2) was measured by radioimmunoassay. Results HT-29 cells were incubated with DCA for 6h. COX-2 experssion of cells were increased prominent compared to controls [(64.2±6.2)ng/L vs (7.1±1.9)ng/L]. The level of PGE2 were increased [(23.9±1.3)ng/L vs (10.5±0.9)ng/L]. Nimesulide reduced the proliferation rate or HT-29 induced by DCA over 6 h. Both COX-2 mRNA expression and the level of PGE2 were inhibited by nimesulide and in a concentration-time dependent manner. Conclusion Nimesulide can inhibit the proliferation of HT- 29 human colon cancer cell induced by DCA. Nimesulide can also suppress the expression of COX-2 ,and decrease the production of PGE2. These data provide new insights into the mechanism of its anti cancer properties.
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