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首页> 外文期刊>Journal of Huazhong University of Science and Technology >Effect and Comparison of Sodium Butyrate and Trichostatin A on the Proliferation/Differentiation of K562
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Effect and Comparison of Sodium Butyrate and Trichostatin A on the Proliferation/Differentiation of K562

机译:丁酸钠和曲古他汀A对K562细胞增殖/分化的影响和比较

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In order to explore the molecular mechanisms of sodium butyrate and trichostatin A on K562 cell proliferation/differentiation, K562 cells were grown in the absence or presence of sodium butyrate or trichostatin A. The percentage of viable cells was determined by trypan blue exclusion. Differentiation was determined by nitro-blue tetrazolium (NBT) reduction and cell surface adhesion molecules analyzed by FACS. Cell cycle distribution was studied after DNA staining by propidium i-odide. Cell cycle regulatory proteins were detected by Western blot and reverse transcription-poly-merase chain reaction. The results showed that sodiun butyrate blocked cells mainly at the G0/G1 phase of the cell cycle, whereas trichostatin A arrested the cells at G2 phase. Sodium butyrate could down-regulate the mRNA expression of cyclin D1 , but not affect its protein expression; down-regulate the protein expression of cyclin D3, but not affect its mRNA expression. Trichostatin A showed similar effects on cyclin Dl and D3 as sodium butyrate. Both sodium butyrate and trichostatin A could stimulate p21 expression of K562 cells at mRNA and protein levels. It may be concluded that sodium butyrate and trichostatin A could promote the proliferation/differentiation of the K562 cells, which might be contributed to the induced expression of cyclin D3 and p21 proteins.
机译:为了探索丁酸钠和曲古抑菌素A对K562细胞增殖/分化的分子机制,在不存在或存在丁酸钠或曲古抑菌素A的情况下培养K562细胞。通过锥虫蓝排除法测定存活细胞的百分比。通过硝基蓝四唑(NBT)还原确定分化,并通过FACS分析细胞表面粘附分子。用碘化丙啶对DNA染色后,研究了细胞周期分布。通过蛋白质印迹和逆转录聚合酶链反应检测细胞周期调节蛋白。结果表明,丁酸丁酯主要在细胞周期的G0 / G1期阻断细胞,而曲古抑菌素A在G2期阻止细胞。丁酸钠可以下调细胞周期蛋白D1的mRNA表达,但不影响其蛋白表达。下调细胞周期蛋白D3的蛋白表达,但不影响其mRNA表达。曲古抑素A对细胞周期蛋白D1和D3显示出与丁酸钠相似的作用。丁酸钠和曲古抑菌素A均可在mRNA和蛋白水平上刺激K562细胞的p21表达。可以得出结论,丁酸钠和曲古抑菌素A可以促进K562细胞的增殖/分化,这可能是诱导细胞周期蛋白D3和p21蛋白表达的原因。

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