Sun Yun-Yu, Wang Shu-Jun, Chen Bao-An, Xia Guo-Hua, Ding Jia-Hua, Gao Chong, Song Hui-Hui, Guo Qing-Long, Zhang Hai-Wei, Li Chun-Rui, Zhou Jian-Feng
Department of Hematology, Southeast University Medical School, Nanjing, Jiangsu Province, China.
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2013 Feb;21(1):105-9. doi: 10.7534/j.issn.1009-2137.2013.01.022.
The aim of this study was to explore the effect of gambogic acid (GA) on MDS SKM-1 cell proliferation, apoptosis and their possible mechanism. Cell proliferation was determined by MTT method. The apoptosis percentage and cell cycle regulation of SKM-1 cells were analyzed by flow cytometry. Morphological features were observed by light microscopy. The mRNA expression of bcl-2 and bax were detected by RT-PCR. The results showed that GA could inhibit the proliferation of SKM-1 cells in a dose- and time-dependent manner (IC50 was 0.37 µg/ml at 48 h), increase the apoptotic percentage of SKM-1 cells, and arrest cell cycle at the G0/G1. The expression of bax mRNA was up-regulated while that of bcl-2 mRNA was down-regulated in SKM-1 cells treated with GA for 48 h. It is concluded that GA can induce apoptosis, which may be related to its effect of arresting cells at phase of G0/G1 and down-regulating bcl-2/bax ratio.
本研究旨在探讨藤黄酸（GA）对骨髓增生异常综合征SKM-1细胞增殖、凋亡的影响及其可能机制。采用MTT法检测细胞增殖情况。通过流式细胞术分析SKM-1细胞的凋亡率和细胞周期调控。用光镜观察形态学特征。采用RT-PCR检测bcl-2和bax的mRNA表达。结果显示，GA能以剂量和时间依赖性方式抑制SKM-1细胞增殖（48 h时IC50为0.37 μg/ml），增加SKM-1细胞的凋亡率，并使细胞周期阻滞于G0/G1期。GA处理48 h的SKM-1细胞中，bax mRNA表达上调，而bcl-2 mRNA表达下调。结论：GA可诱导细胞凋亡，这可能与其使细胞阻滞于G0/G1期及下调bcl-2/bax比值的作用有关。
