Ursolic Acid Inhibits T-Cell Activation through Modulating Nuclear Factor-κB Signaling

来源 :Chinese Journal of Integrative Medicine | 被引量 : 0次 | 上传用户:donglaoshi_imnu
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Objective:To investigate the effects of ursolic acid(UA) on T-cell proliferation and activation,as well as to examine its effect on nuclear factor-κB(NF-κB) signaling pathway in T cells.Methods:T-cells isolated from BALB/c mice were incubated with UA at concentrations ranging from 5-30μmol/L in the presence of phorbol 12-myristate 13-acetate(PMA) or PMA plus ionomycin.The proliferation of T cells was measured by the MTT assay.The expressions of CD69,CD25,and CD71 on T-cell surface were analyzed using flow cytometry. The level of interleukin-2(IL-2) in the culture supernatant of activated T cells was quantified by enzyme-linked immunosorbent assay(ELISA).The level of phosphorylated IκB-α(p-lκB-α) in total protein and p65,a subunit of NF-κB,nuclear translocation were measured by Western blot analysis.Results:UA in a dose-dependent manner significantly decreased the proliferation and inhibited the surface expressions of CD69,CD25,and CD71 in murine T lymphocytes upon in vitro activation(P<0.01).Significant reduction of IL-2 production was found in activated T cells treated with UA(P<0.01).The PMA-induced increase in p-lκB-αprotein was inhibited,and nuclear translocation of p65 from the cytoplasm was blocked by UA.Conclusion:UA is a potent inhibitor for T cell activation and proliferation;these effects are associated with the inhibition of NF-κB signaling pathway. Objective: To investigate the effects of ursolic acid (UA) on T-cell proliferation and activation, as well as to examine its effect on nuclear factor-κB (NF-κB) signaling pathway in T cells. Methods: T-cells isolated from BALB / c mice were incubated with UA at concentrations ranging from 5-30 μmol / L in the presence of phorbol 12-myristate 13-acetate (PMA) or PMA plus ionomycin. The proliferation of T cells was measured by the MTT assay. The levels of interleukin-2 (IL-2) in the culture supernatant of activated T cells were quantified by enzyme-linked immunosorbent assay (ELISA) of CD69, CD25, and CD71 on T-cell surface were analyzed using flow cytometry. level of phosphorylated IκB-α (p-lκB-α) in total protein and p65, a subunit of NF-κB, nuclear translocation were measured by Western blot analysis. Results: UA in a dose-dependent manner significantly decreased the proliferation and inhibited the surface expressions of CD69, CD25, and CD71 in murine T lymphocytes upon in vitro acti Vation (P <0.01) .Significant reduction of IL-2 production was found in activated T cells treated with UA (P <0.01). PMA-induced increase in p-IκB- αprotein was inhibited, and nuclear translocation of p65 from the cytoplasm was blocked by UA.Conclusion: UA is a potent inhibitor for T cell activation and proliferation; these effects are associated with the inhibition of NF-κB signaling pathway.
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