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异硫氰酸苯己酯对体外诱导多发性骨髓瘤细胞凋亡的作用

[Effect of phenylhexyl isothiocyanate on inducing apoptosis of multiple myeloma cells in vitro].

作者信息

Lu Quan-Yi, Wang Zhao, Liu De-Long

机构信息

Department of Hematology, Zhongshan Hospital of Xiamen, Fujian Medical University, Xiamen 361004, Fujian Province, China.

出版信息

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2008 Feb;16(1):89-92.

Abstract

In order to investigate the effects of phenylhexyl isothiocyanate (PHI) on proliferation and apoptosis of multiple myeloma cells RPMI8226 in vitro, the RMPI8226 cells were co-cultured with PHI at various concentrations; the apoptosis of PHI-treated cells was assayed by TUNEL; the cell cycle changes of PHI-treated cells were analyzed by FCM; the mitochondrial potential changes of PHI-treated cells were detected by using a potential sensitive dye JC-1 as probe; the VEGF levels secreted from PHI-treated cells were measured by quantitative sandwich ELISA. The results showed that PHI significantly inhibited RPMI8226 cell proliferation, induced their apoptosis at low concentration (0.5 micromol/L), the inhibitory effect was related to PHI concentration. PHI-treated cells were arrested in G(0)/G(1) phase. The RPMI8226 cells showed shift from red fluorescence to green fluorescence in some concentration-dependent manner, indicating increase of mitochondrial depolarization and potential loss by 3-4-fold as compared with control, after treated RMPI8226 cells with 10 micromol/L of PHI for 48 hours, the VEGF level secreted from RMPI8226 cells significantly decreased, it was 35% of control. It is concluded that the PHI can inhibit cell proliferation, induce cell apoptosis of RMPI8226, the cell apoptosis is associated with mitochondrial depolarization and potential loss, the inhibiting VEGF secretion from RMPI8226 cells by PHI may be one of the reasons causing apoptosis. PHI may be a potential therapeutic drug for multiple myeloma.

摘要

为了研究异硫氰酸苯己酯(PHI)对体外多发性骨髓瘤细胞RPMI8226增殖和凋亡的影响,将RMPI8226细胞与不同浓度的PHI共培养;采用TUNEL法检测经PHI处理细胞的凋亡情况;通过流式细胞术分析经PHI处理细胞的细胞周期变化;以电位敏感染料JC-1为探针检测经PHI处理细胞的线粒体电位变化;采用定量夹心ELISA法测定经PHI处理细胞分泌的VEGF水平。结果显示,PHI显著抑制RPMI8226细胞增殖,在低浓度(0.5微摩尔/升)时诱导其凋亡,抑制作用与PHI浓度有关。经PHI处理的细胞停滞于G(0)/G(1)期。RPMI8226细胞呈现出一定浓度依赖性的从红色荧光向绿色荧光的转变,表明与对照组相比,线粒体去极化增加且电位损失增加3至4倍,用10微摩尔/升的PHI处理RPMI8226细胞48小时后,RPMI8226细胞分泌的VEGF水平显著降低,为对照组的35%。结论是,PHI可抑制RPMI8226细胞增殖,诱导其细胞凋亡,细胞凋亡与线粒体去极化和电位损失有关,PHI抑制RPMI8226细胞分泌VEGF可能是导致凋亡的原因之一。PHI可能是一种潜在的多发性骨髓瘤治疗药物。

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