sq-23377 and arctigenin

This study investigated the effect of arctigenin (Arc) on the cell activation, cytokines expression, proliferation, and cell-cycle distribution of mouse T lymphocytes. Mouse lymphocytes were prepared from lymph node and treated with Phorbol-12-myristate-13-acetate (PMA)/Ionimycin (Ion) and/or Arc. CD69, CD25, cytokines, proliferation and cell cycle were assayed by flow cytometry. The results showed that, at concentrations of less than 1.00 micromol x L(-1), Arc expressed non-obvious cell damage to cultured lymphocytes, however, it could significantly down-regulate the expression of CD69 and CD25, as well as TNF-alpha, IFN-gamma, IL-2, IL-4, IL-6 and IL-10 on PMA/Ion stimulated lymphocytes. At the same time, Arc could also inhibit the proliferation of PMA/Ion-activated lymphocytes and exhibited lymphocyte G 0/G1 phase cycle arrest. These results suggest that Arc possesses significant anti-inflammatory effects that may be mediated through the regulation of cell activation, cytokines expression and cell proliferation.

Topics: Animals; Anti-Inflammatory Agents; Antigens, CD; Antigens, Differentiation, T-Lymphocyte; Arctium; Cell Cycle Checkpoints; Cell Proliferation; Cytokines; Female; Furans; Interferon-gamma; Interleukin-10; Interleukin-2; Interleukin-2 Receptor alpha Subunit; Interleukin-4; Interleukin-6; Ionomycin; Lectins, C-Type; Lignans; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Plants, Medicinal; T-Lymphocytes; Tetradecanoylphorbol Acetate; Tumor Necrosis Factor-alpha