Aim:To investigate the antiproliferative effect of triptolide on B-NHL cell line Rajicells,to study its effect on lymph node metastasis in patients with non-Hodgkin’slymphoma(NHL)in vitro,and to explore the underlying mechanism regulatingSDF-1/CXCR4 axis.Methods:The effects of triptolide on the growth of Raji cellswere studied by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium(MTT)assay.The effects of triptolide on SDF-1 mRNA expression in lymph node stromalcells from patients with NHL were determined by reverse transcriptase-polymerasechain reaction(RT-PCR).The effects of triptolide on CXCR4 expression on lym-phoma cells freshly isolated from the lymph nodes of these patients were studiedby flow cytometric analysis.Chemotaxis assays were performed to observe theeffects of triptolide on migration of primary lymphoma cells towards recombinanthuman SDF-1α(rhSDF-1α)or cultured lymph node stromal cells in vitro.Results:Triptolide inhibited the proliferation of B-NHL cell line Raji cells in a dose-andtime-dependent manner with a 24-h IC_(50)value of 43.06 nmol/L and a 36-h IC_(50)valueof 25.08 nmol/L.The expression of SDF-1α mRNA in lymph node stromal cellsobtained from patients with NHL was decreased after treatment by triptolide atconcentrations of 25 and 50 nrnol/L for 24 h.Flow cytometry analysis showed thatthe CXCR4 expression on primary lymphoma cells were downregulated graduallyin a dose-dependent manner following triptolide treatment.Chemotaxis assaysrevealed that the migration of freshly isolated lymphoma cells towards either rhSDF-1or cultured lymph node stromal cells was markedly inhibited by the addition oftriptolide in vitro,and the inhibition was dose-dependent.Conclusion:Triptolidecan inhibit the proliferation of B-NHL cell line Raji cells.Moreover,triptolide isable to inhibit the migration of lymphoma cells via lymph nodes in vitro.Thepotential antitumor mechanisms of triptolide are related to the antiproliferativeeffect and the blockage of SDF-1/CXCR4 axis. Aim: To investigate the antiproliferative effect of triptolide on B-NHL cell line Rajicells, to study its effect on lymph node metastasis in patients with non-Hodgkin’s lymphoma (NHL) in vitro, and to explore the underlying mechanism regulating SDF-1 / CXCR4 axis. Methods: The effects of triptolide on the growth of Raji cells were studied by 3- (4,5-dimethyl-2-thiazolyl) -2,5-diphenyl-2H- tetrazolium (MTT) assay. The effects of triptolide on SDF -1 mRNA expression in lymph node stromal cells from patients with NHL were determined by reverse transcriptase-polymerasechain reaction (RT-PCR). The effects of triptolide on CXCR4 expression on lym-phoma cells freshly isolated from the lymph nodes of these patients were studied by flow cytometric analysis. Chemotaxis assays were performed to observe the effects of triptolide on migration of primary lymphoma cells towards recombinant human SDF-1α (rhSDF-1α) or cultured lymph node stromal cells in vitro. Results: Triptolide inhibited the proliferation of B-NHL cell line Raji cells in a dose-and-time dependent manner with a 24-h IC 50 value of 43.06 nmol / L and a 36-h IC 50 value of 25.08 nmol / L The expression of SDF-1α mRNA in lymph node stromal cellsobtained from patients with NHL was decreased after treatment by triptolide at concentrations of 25 and 50 nrnol / L for 24 h. Flow cytometry analysis showed that the CXCR4 expression on primary lymphoma cells were downregulated gradually in a dose-dependent manner following triptolide treatment. Chemotaxis assaysrevealed that the migration of freshly isolated lymphoma cells either either rhSDF-1or cultured lymph node stromal cells was markedly inhibited by the addition oftriptolide in vitro, and the inhibition was dose-dependent. Confc: Triptolidecan inhibit the proliferation of B-NHL cell line Raji cells. Furthermore, triptolide is able to inhibit the migration of lymphoma cells via lymph nodes in vitro. The potential antitumor mechanisms of triptolide are related to the antiproliferative effect and the blockage of SDF-1 / CXCR4 axis.