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拓扑特肯诱导人口腔上皮癌细胞凋亡的机制
http://www.100md.com 《第四军医大学学报》 2004年第16期
人口腔上皮癌细胞株,,拓扑特肯;人口腔上皮癌细胞株;磷酸化的丝裂原活化蛋白激酶38;凋亡,0引言,1材料和方法,2结果,3讨论,【参考文献】
     Mechanism of apoptosis of KB cells induced by Topotecan (TPT)

    XU Qiang, WANG Feng, LI DengSong, CHEN ChangSheng, XU Wen, MIAO Shan

    1Department of Stomatology, Lanxi Railway Hospital, Lanzhou 730050, 2Department of Nutrition & Food Hygiene, School of Preventive Medicine, Fourth Military Medical University, Xian 710033, China, 3Military Medical Institute of Lanzhou Command, 4Department of Statistics, 5Department of Toxicology, School of Preventive Medicine, Fourth Military Medical University, Xian 710033, China, 6Institute of Materia Medica, Administration of Scientific Research, Fourth Military Medical University, Xian 710033, China

    【Abstract】 AIM: To study the mechanism of apoptosis of KB cells induced by Topotecan (TPT). METHODS: MTT assay was applied to test the proliferation arrest of KB cells under the treatment of TPT for 12, 24 and 48 h, agarose gel electrophoresis of genomic DNA and flow cytometry (FCM) were used to examine the apoptosis of TPTtreated KB cells and Westernblot was used to test the phosphorylations of p38MAPK proteins. RESULTS: The inhibition ratio of TPTtreated KB cells for 12, 24 and 48 h was (24.4±9.1)%, (33.7±6.6)% and (45.1±10.4)%, respectively, with significant difference between different treatment duration (P<0.05). By FCM, the apoptosis rate of the cells was (11.5±2.8)% at 12h and (31.2±4.1)% at 24 h, with significant difference (P<0.01). Agarose gel electrophoresis of genomic DNA of TPTtreated KB cells for 12 h showed DNA fragmentations, typical index of apoptosis in biochemistry. The phosphorylations of p38 increased gradually with the prolongation of TPT treatment (12, 24 and 48 h) (n=3, P<0.05). CONCLUSION: TPTinduced apoptosis of KB cells in vitro may result from the enhanced activation of p38MAPK. ......

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