Astilbin suppresses acute heart allograft rejection by inhibiting maturation and function of dendritic cells in mice.

The effect of astilbin on acute graft rejection was investigated in C57BL/6 mice carrying BALB/c hearts heterotopically transplanted into the neck vessels. Daily treatment with astilbin (50, 125, or 250 mg/kg intraperitoneally) significantly prolonged the survival of grafts in a dose-dependent manner, when cyclosporine (CsA; 5 mg/kg) was co-administered with astilbin (250 mg/kg), there was more potent immunosuppression than that solely achieved by 20 mg/kg CsA. Addition of 10 mg/mL astilbin significantly inhibited the proliferation and activation of T cells, as determined by (3)H-thymidine deoxyribose uptake, Western blots for nuclear factor κB and p38, and 1-way mixed lymphocyte reactions (MLR). Mature and antigen-presenting functions of dendritic cells (DCs) also were inhibited by astilbin (10 mg/mL), as determined by morphologic observations, flow cytometry, and MLR. These observations suggested that astilbin is a potential candidate for immunosuppressive therapy after heart engraftment. Inhibiting the maturation and antigen-presenting function of DCs and thus preventing T-cells activation is a possible mechanism underlying its inhibitory effects on acute heart allograft rejection.