Objective: The co-culture system of mouse spleen lymphocytes(SLs) and colon cancer CT26.WT cell were used to study the influence of emodin on nuclear factor-κB(NF-κB) pathways in tumor cells

and to explore the anti-tumor mechanism of emodin. Method: 1×105/mL CT26 cells and spleen lymphocytes(SLs) were mixed according to the 1:1

1:2

1:4 ratio

and incubated for 24 h

which was cultured with emodin of different concentration (10

20

40

80 mmol·L-1)for 4 h. The expression of chemokine C-C mofif chemokine ligand 17(CCL17) in CT26 cells

the expression ratio of chemokine receptor C-C motif chemokine receptor 4(CCR4) on SLs surface and the levels of CCR4 mRNA

NF-κB activation in CT26 cells were detected. Result: CCL17 was detected in the mixed groups(P<0.01). CCL17 was markedly inhibited in the mixed group by emodin from 308 ng·L-1 to 124 ng·L-1 in 1:1 group. Emodin had no effect in CCR4+CD4+CD25+ Tregs in SLs group.But CCR4 expression of CD4+CD25+ Tregs was decreased significantly in mixed group from 44.58% to 32.86% in 1:4 group similar to those CCR4 mRNA expression (P<0.05). Emodin markedly inhibited the activation of NF-κB of CT26 cells (P<0.05)

and the mean fluorescence values of p65 from 358 (0 mmol·L-1) to 76 (80 mmol·L-1). Conclusion: Emodin can reduce the secretion of CCL17 in CT26 cell

and decrease significantly the CCR4 expression of regulatory Treg cell surface and the expression of mRNA level;emodin markedly inhibit activation of NF-κB in CT26 cells.