Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (53): 10003-10006.doi: 10.3969/j.issn.1673-8225.2011.53.030

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Effects of tacrolimus on the proliferation of HepG2.2.15 cells and the replication of hepatitis B virus in vitro

Wang Jian, Shen Zhong-yang, Song Hong-li, Zheng Wei-ping, Song Xiao-jing   

  1. Organ Transplantation Center, Tianjin First Central Hospital, Tianjin  300192, China
  • Received:2011-05-18 Revised:2011-08-01 Online:2011-12-31 Published:2011-12-31
  • Contact: Song Hong-li, Doctor, Chief physician, Organ Transplantation Center, Tianjin First Central Hospital, Tianjin 300192, China hlsong26@yahoo.com.cn
  • About author:Wang Jian★, Master, Organ Transplantation Center, Tianjin First Central Hospital, Tianjin 300192, China wangjian88@medmail.com.cn
  • Supported by:

    Science and Technology Foundation Program of Health Bureau of Tianjin, No. 05KYZ24*, 2011KY11*; Basic Key Project of Tianjin Committee of Science and Technology, No. 11JCZDJC27800*

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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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