Melatonin and Doxorubicin synergistically induce cell apoptosis in human hepatoma cell lines
Melatonin and Doxorubicin synergistically induce cell apoptosis in human hepatoma cell lines
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褪黑素和阿霉素协同诱导人肝癌细胞系细胞凋亡
DOI：
10.3748/wjg.v16.i12.1473
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发表时间：
2010-03-28
影响因子：
4.3
通讯作者：
Wang, Hua
中科院分区：
文献类型：
--
作者：
Fan, Lu-Lu;Sun, Guo-Ping;Wang, Hua
目的：探讨褪黑素与阿霉素在抑制人肝癌细胞株HepG2和Bel-7402生长和诱导凋亡中的协同作用。方法：褪黑素与阿霉素协同作用抑制人肝癌细胞株HepG2和Bel-7402细胞生长，诱导细胞凋亡。采用3-（4,5-二甲基噻唑-2-基）-2,5-二苯基溴化四唑（MU）法测定细胞活力。采用TUNEL法和流式细胞术观察细胞凋亡情况。免疫组化染色检测凋亡相关蛋白Bax、Bcl-2、caspase-3的表达。结果：单独使用褪黑素(10（-8)-10(-5)mol/L）对肝癌细胞系HepG2和Bel-7402具有剂量相关的细胞增殖抑制作用，但对其没有细胞毒性作用。有趣的是，当与阿霉素联合使用时，褪黑素显著增加了细胞生长抑制和细胞凋亡的作用。此外，TUNEL染色和流式细胞术显示，协同诱导凋亡与Bcl-2表达降低以及Bax和Caspase3表达升高有关。结论：褪黑素与阿霉素协同作用可抑制肝癌细胞生长，诱导细胞凋亡。(C) 2010年白石登。版权所有。
AIM: To investigate whether Melatonin has synergistic effects with Doxorubicin in the growth-inhibition and apoptosis-induction of human hepatoma cell lines HepG2 and Bel-7402.METHODS: The synergism of Melatonin and Doxorubicin inhibited the cell growth and induced cell apoptosis in human hepatoma cell lines HepG2 and Bel-7402. Cell viability was analyzed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MU) assay. Cell apoptosis was evaluated using TUNEL method and flow cytometry. Apoptosis-related protein Bax, Bcl-2 and caspase-3 expressions were measured by immunohistochemical staining.RESULTS: Treatment with Melatonin (10(-8)-10(-5) mol/L) alone had a dose-related inhibitory effect on cell proliferation but no cytotoxic effect on hepatoma cell lines HepG2 and Bel-7402. Interestingly, when combined with Doxorubicin, Melatonin significantly increased the effects of cell growth inhibition and cell apoptosis. Furthermore, TUNEL staining and flow cytometry revealed that cooperative apoptosis induction was associated with decreased expression of Bcl-2 as well as increased expression of Bax and Caspase3.CONCLUSION: The synergism of Melatonin and Doxorubicin inhibits hepatoma cell growth and induces cell apoptosis. (C) 2010 Baishideng. All rights reserved.