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. 2012 Oct;25(5):368–378. doi: 10.1089/vim.2012.0008

Table 4.

Effects of Different Concentrations of MP and FK506 on cccDNA in HepG2.2.15 Cells (n=3)

 
 
HBV cccDNA (copies/mL)
Medication Concentration (μg/L) 24 h 48 h 72 h
MP 0(1) 6.9279±0.0278 6.9480±0.0119 6.8164±0.0752
MP 10(2) 6.2319±0.4287 5.9526±0.0454 5.8975±0.0295
MP 50(3) 6.1858±0.7162 5.5906±0.1751 5.7471±0.0524
MP 100(4) 5.7439±0.8762 5.5800±0.0979 5.1162±0.0038
MP 250(5) 5.1583±0.3957 5.1427±0.3142 4.8272±0.0364
  F 3.956* 49.283** 842.499**
  r −0.762 −0.902 −0.972
  p 0.001 0.000 0.000
FK506 0(1) 6.2142±0.1357 6.3327±0.0224 6.3972±0.0824
FK506 50(2) 5.9847±0.1808 5.9449±0.2451 6.4222±0.1501
FK506 100(3) 6.0663±0.0502 5.8854±0.2664 5.7476±0.3293
FK506 500(4) 5.59033±0.0449 5.6382±0.4164 5.5517±0.6007
  F 3.791 3.251 4.790
*

p<0.05; **p<0.01.

HepG2.2.15 cells were treated with different concentrations of MP and FK506. The cccDNA levels were significantly decreased by MP in a concentration-dependent (but time-independent) manner compared with the control group (r=−0.957, −0.927, −0.917; p≤0.001). FK506 had no inhibitory effect on cccDNA replication in vitro (p>0.05).

MP, methylprednisolone; FK506, tacrolimus; HBV, hepatitis B virus; cccDNA, covalently-closed circular DNA.