Immunosuppressive effects of ginsenoside-Rd on skin allograft rejection in rats.

Organ transplantation is a life-saving procedure for patients with organ failure. However, the side effects of long-term application of classic immunosuppressant remain major obstacles for successful transplantation. Therefore, new and safe immunosuppressive drugs against acute and chronic rejection are eagerly awaited. In the present study, we detected the effect of ginsenoside-Rd on mitogen-induced mouse spleen lymphocytes proliferation in vitro and observed the effect of ginsenoside-Rd on allograft rejection in a rat skin transplantation model. Th1/Th2 type cytokines secretion and T-cell subsets were also detected. The results showed that ginsenoside-Rd could markedly inhibit Concanavalin A (ConA)-induced mouse spleen T lymphocytes proliferation. Also, ginsenoside-Rd could significantly prolong the mean survival time of skin allograft and improve the skin allograft pathological damage. Furthermore, ginsenoside-Rd could markedly suppress alloantigen-specific production of Th1 cytokines IL-2 and IFN-γ as well as proinflammatory cytokines TNFα and IL-12. In parallel, Th2 cytokine IL-10 production in serum of rat recipients was markedly up-regulated. Ginsenoside-Rd at a dose of 25 mg/kg could significantly reduce the percentages of CD4(+) T cells and CD8(+) T cells in peripheral blood of rat recipients. Our results suggest that ginsenoside-Rd can effectively antagonize transplant rejection, which might qualify ginsenoside-Rd as a putative, therapeutic drug for the treatment of Th1-driven diseases, including transplant rejection.