Sodium tanshinone IIA sulfonate prolongs the survival of skin allografts by inhibiting inflammatory cell infiltration and T cell proliferation

• We found that STS has an immunosuppressive effect in a rat skin transplantation model.
• STS inhibits inflammatory cell infiltration and Th1 cytokine secretion.
• The proliferation of T cells can be inhibited by STS.
• STS may serve as a new therapeutic alternative for allograft rejection.

Acute rejection is a major problem for allograft transplantation in the clinic. Classic immunosuppressive drug therapy is accompanied by a variety of side effects. Therefore, safe and effective immunosuppressive drugs remain in demand. In this study, the effect of sodium tanshinone IIA sulfonate (STS) on prolonging the allogeneic skin graft survival was determined using a rat skin transplantation model. Rat recipients were divided into four groups that received different treatments: physiological saline, STS, CsA, or STS + CsA. The results indicated that the administration of STS alone, CsA alone or combined STS and CsA all significantly promoted skin allograft survival as demonstrated by a longer mean survival time (MST) compared with the control group. This effect was due to the reductions in the infiltration of inflammatory cells into allograft and the percentages of CD4 + T cells and CD8 + T cells in the peripheral blood of rat recipients. The injection of STS could also downregulate the expression of RANTES, IP-10 as well as IL-2, IFN-γ and TNF-α in allograft tissue. STS markedly inhibited the proliferation of mouse spleen T lymphocytes stimulated by mitogen and alloantigen in vitro. Taken together, these results suggest that STS is a widely applicable drug with few complications that may serve as a new therapeutic alternative for allograft rejection or even other Th1 cell-dominated immune diseases.