| 他克莫司在体外对HepG2.2.15细胞增殖及乙型肝炎病毒复制的影响 |
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| 引用本文： | 王 建,沈中阳,宋红丽,郑卫萍,宋晓静. 他克莫司在体外对HepG2.2.15细胞增殖及乙型肝炎病毒复制的影响[J]. 中国组织工程研究, 2011, 15(53): 10003-10006. DOI: 10.3969/j.issn.1673-8225.2011.53.030 |
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| 作者姓名： | 王 建 沈中阳 宋红丽 郑卫萍 宋晓静 |
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| 作者单位： | 天津市第一中心医院器官移植中心,天津市 300192 |
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| 基金项目： | 天津市卫生局科技基金资助项目(05KYZ24,2011KY11);天津市科委基础重点课题资助项目(11JCZDJC27800)。 |
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| 摘 要： | 背景：肝癌复发与乙肝病毒再感染两者关系尚不明确,有人认为与肝移植后免疫抑制剂应用有关。目的：观察他克莫司在体外对肝癌HepG2.2.15细胞增殖及对细胞内乙肝病毒复制的影响。方法：选择肝癌HepG2.2.15细胞进行体外培养,第3代细胞培养24 h后加他克莫司进行干预,0 g/L他克莫司作为对照组,50 g/L 他克莫司为低浓度组,100,500 g/L他克莫司为中浓度组,1 000,3 000 g/L他克莫司为高浓度组。结果与结论：①中、高浓度的他克莫司对HepG2.2.15细胞有增殖抑制作用,低浓度无抑制作用,且有相关性。②高浓度他克莫司作用时使HepG2.2.15细胞停止在G0/G1期。③他克莫司可以使HepG2.2.15细胞中CyclinA表达降低,且呈浓度依赖性,他克莫司浓度越高,CyclinA表达越少。④他克莫司作用HepG2.2.15细胞,对HBV的复制无影响。结果说明他克莫司在体外对HepG2.2.15增殖有抑制作用,其中CyclinA可能发挥一定的作用,而对乙肝病毒复制没有影响。
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| 关 键 词： | 他克莫司 HepG2.2.15细胞 Cyclin A 乙型肝炎病毒 增殖 复制 |
| 收稿时间： | 2011-05-18 |
Effects of tacrolimus on the proliferation of HepG2.2.15 cells and the replication of hepatitis B virus in vitro |
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| Wang Jian,Shen Zhong-yang,Song Hong-li,Zheng Wei-ping,Song Xiao-jing. Effects of tacrolimus on the proliferation of HepG2.2.15 cells and the replication of hepatitis B virus in vitro[J]. Chinese Journal of Tissue Engineering Research, 2011, 15(53): 10003-10006. DOI: 10.3969/j.issn.1673-8225.2011.53.030 |
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| Authors: | Wang Jian Shen Zhong-yang Song Hong-li Zheng Wei-ping Song Xiao-jing |
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| Affiliation: | Organ Transplantation Center, Tianjin First Central Hospital, Tianjin 300192, China |
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| Abstract: | BACKGROUND:The relationship between liver cancer recurrence and hepatitis B virus recurrence remains poorly understood and it is considered to be related to application of immunosuppressive agent after liver transplantation. OBJECTIVE:To investigate the effects of tacrolimus (FK506) on the proliferation of HepG2.2.15 cells and the replication of hepatitis B virus in vitro. METHODS:HepG2.2.15 cells were in vitro cultured. After passage 3 HepG2.2.15 cells were cultured for 24 hours, they were interfered with different concentrations of FK506. 0 g/L FK506-interfered group served as control group, 50 g/L FK506-interfered group as low-concentration FK506 group, 100 g/L or 500 g/L FK506-interfered group as medium-concentration FK506 group, and 1 000 g/L or 3 000 g/L FK506-interfered group as high-concentration FK506 group. RESULTS AND CONCLUSION:Moderate- and high-concentration FK506 exhibited inhibitory effects on the proliferation of HepG2.2.15 cells, while low-concentration FK506 exhibited no inhibitory effects with correlation. High-concentration FK506 made HepG2.2.15 cells arresting at G0/G1 stage. FK506 decreased CyclinA expression in HepG2.2.15 cells in a dose-dependent manner. Higher concentration of FK506 leaded to lower expression of CyclinA. FK506 did not produce effects on the replication of hepatitis B virus in HepG2.2.15 cells. These results indicate that FK506 inhibits the proliferation of HepG2.2.15 cells in vitro, which occurs possibly due to Cyclin A, but it would not affect the replication of hepatitis B virus in vitro. |
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