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- κ B （NF- κ B） signaling pathway in T cells. Methods： T-cel...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- κ B （NF- κ B） 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 MIF 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 I κ B-α （p-I κ B-α ） in total protein and p65, a subunit of NF- κ B, 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-I κ B-α protein 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- κ B signaling pathway.展开更多
基金Supported by the Natural Science Foundation of China(No. 30371833)the Science and Technology Project Foundation of Hunan Science and Technology Bureau(No.2007SK3030)
文摘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- κ B （NF- κ B） 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 MIF 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 I κ B-α （p-I κ B-α ） in total protein and p65, a subunit of NF- κ B, 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-I κ B-α protein 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- κ B signaling pathway.
