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作 者:欧学平[1] 肖翠翠[1] 宋萌[1] 肖忠明[2] 韦芳[2] 洪艳[2]
机构地区:[1]上海交通大学附属上海第一人民医院口腔科,上海200080 [2]上海交通大学附属上海第一人民医院实验中心,上海200080
出 处:《口腔颌面外科杂志》2012年第3期163-167,共5页Journal of Oral and Maxillofacial Surgery
基 金:上海市科学技术委员会资助项目(08JC1412900);上海市重点学科建设项目(S30206-KF05)
摘 要:目的:探讨环杷明(cyclopamine)诱导人腮腺多形性腺瘤细胞凋亡的作用及其对Gli-2和Bcl-2表达的影响。方法:用10μmol∕L环杷明处理人腮腺多形性腺瘤细胞,48 h后倒置显微镜下观察细胞数量及形态变化;48 h后实时定量PCR检测实验组(环杷明组)和空白对照组、DMSO对照组的Gli-2、Bcl-2 mRNA表达水平差异;24 h后流式细胞术观察细胞凋亡。结果:人腮腺多形性腺瘤细胞用10μmol∕L环杷明作用48 h后倒置显微镜下可见细胞数量减少、细胞核固缩或碎裂、核仁变形等典型的细胞凋亡形态学变化;环杷明组与空白对照组、DMSO对照组相比,可以显著下调Gli-2、Bcl-2 mRNA表达(P<0.01);环杷明组的细胞凋亡率明显高于空白对照组和DMSO对照组(P<0.01)。结论:环杷明可诱导人腮腺多形性腺瘤细胞凋亡,其作用机制可能与下调Gli-2、Bcl-2 mRNA表达,活化细胞凋亡的线粒体途径有关。Objective: The purpose of this study was to examine whether cyclopamine is related to apoptosis and growth inhibition of human salivary pleomorphic adenoma (HSPA) cells. Methods: HSPA cells were treated with cyclopamine. Observed the cells quantity change and morphology after 48 h. Cells cultured with DMSO 0.08% or void were used as control. Gli-2 and Bcl-2 mRNA expression was examined by Real-time PCR after 48 h. Flow eytometry was used to analyze cell apoptosis after 24 h. Experiment results are presented as x^-±s. Statistical analysis was undertaken with SAS 9.13. The differences among the groups were identified by one-way ANOVA. Significance was accepted at P〈0.01. Result: The number of eyclopamine treated HSPA cells was significantly decreased. Cyclopamine treated (10 μmol/L) HSPA cells showed nuclear psychosis or fragmentation, chromatospherite disfiguration with apoptoticmorphology. The expression levels of Gli-2 and Bel-2 mRNA in 10/J, mol / L cyelopamine treated group was down-regulated significantly compare with blank and DMSO control groups (P〈0.01). Apoptosis rate of 10μ mol / L cyclopamine treatment group was significantly higher than blank and DMSO control group (P〈0.01). Conclusion: Cyclopamine appears to induce growth inhibition and apoptosis in human salivary pleomorphie adenoma cells. The mechanism may be related to down-regulation of Gli-2 and Bcl-2 mRNA, which activates the mitochondrial apoptotic pathways.
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