航天医学与医学工程
航天醫學與醫學工程
항천의학여의학공정
SPACE MEDICINE & MEDICAL ENGINEERING
2007年
5期
313-316
,共4页
蔡天革%蔡宇%余绍蕾%冯笑珍
蔡天革%蔡宇%餘紹蕾%馮笑珍
채천혁%채우%여소뢰%풍소진
补骨脂素%多药耐药%逆转%MCF-7/ADR细胞
補骨脂素%多藥耐藥%逆轉%MCF-7/ADR細胞
보골지소%다약내약%역전%MCF-7/ADR세포
psoralen%multidrug resistance%reverse%MCF-7/ADR cells
目的 研究补骨脂素对MCF-7/ADR耐药细胞逆转作用及对耐药细胞内Ca2+浓度影响,探讨其可能作用机制.方法 采用MTT法测定补骨脂素对细胞增殖抑制作用,高效液相色谱法检测细胞内ADR的浓度,激光共聚焦显微镜测定细胞内不同时段的Ca2+浓度.结果 补骨脂素在1~20 μmol/L浓度下能不同程度降低ADR对MCF-7/ADR细胞的IC50,并不同程度提高细胞内ADR浓度;1~20 μmol/L补骨脂素在不同作用时段(24、48、96 h)对MCF-7/ADR细胞内Ca2+浓度与作用时间呈负相关.结论 补骨脂素能逆转MCF-7/ADR细胞的MDR,其作用机制与影响耐药细胞内Ca2+浓度,故而增加细胞内ADR浓度有关.
目的 研究補骨脂素對MCF-7/ADR耐藥細胞逆轉作用及對耐藥細胞內Ca2+濃度影響,探討其可能作用機製.方法 採用MTT法測定補骨脂素對細胞增殖抑製作用,高效液相色譜法檢測細胞內ADR的濃度,激光共聚焦顯微鏡測定細胞內不同時段的Ca2+濃度.結果 補骨脂素在1~20 μmol/L濃度下能不同程度降低ADR對MCF-7/ADR細胞的IC50,併不同程度提高細胞內ADR濃度;1~20 μmol/L補骨脂素在不同作用時段(24、48、96 h)對MCF-7/ADR細胞內Ca2+濃度與作用時間呈負相關.結論 補骨脂素能逆轉MCF-7/ADR細胞的MDR,其作用機製與影響耐藥細胞內Ca2+濃度,故而增加細胞內ADR濃度有關.
목적 연구보골지소대MCF-7/ADR내약세포역전작용급대내약세포내Ca2+농도영향,탐토기가능작용궤제.방법 채용MTT법측정보골지소대세포증식억제작용,고효액상색보법검측세포내ADR적농도,격광공취초현미경측정세포내불동시단적Ca2+농도.결과 보골지소재1~20 μmol/L농도하능불동정도강저ADR대MCF-7/ADR세포적IC50,병불동정도제고세포내ADR농도;1~20 μmol/L보골지소재불동작용시단(24、48、96 h)대MCF-7/ADR세포내Ca2+농도여작용시간정부상관.결론 보골지소능역전MCF-7/ADR세포적MDR,기작용궤제여영향내약세포내Ca2+농도,고이증가세포내ADR농도유관.
Objective To research the reversal effects of psoralen on multidrug resistant action and its influence on intracellular Ca2+ concentration in MCF-7/ADR cells and to explore its possible mechanisms of reversing multidrug resistance (MDR). Methods The inhibitory effects of psoralen on the viability of MCF-7/ADR cells were determined with MTT assay, intracellular adriamycin (ADR) concentration was assayed with HPLC and the intracellular Ca2+ concentrations in different incubative duration were detected with confocal microscope. Results Psoralen from 1 to 20 μmol/L reduced the value of IC50 of ADR in MCF-7/ADR cells, enhanced accumulation of ADR and influenced Ca2+ concentration with a negative correlation in different duration (24 h, 48 h and 96 h). Conclusion Psoralen can reverse MDR in MCF-7/ADR cells and its mechanism may be related to the increase of the intracellular accumulation of ADR by enhancing the intracellular Ca2+ concentration.