[Retracted] Rocaglamide Prolonged Allograft Survival by Inhibiting Differentiation of Th1/Th17 Cells in Cardiac Transplantation

Figure 7

Rocaglamide inhibits Th1/Th17 cell differentiation and prolonged graft survival through NF-AT pathway downregulation. (a) Recipients were treated with PBS () and rocaglamide () for survival studies. Heart grafts were monitored until they stopped beating. Grafts were performed, and recipients were sacrificed on day 7 for histological, MLR, ELISA, PCR, and flow cytometric analysis. RNA was extracted from the grafts of recipient mice. (b) Rocaglamides inhibit NF-AT via the activation of MAPKs, and rocaglamide can enhance the phosphorylation of pJNK and p38 in the simulation environment. Rocaglamide suppresses the nuclear expression of NF-AT in activated T cells. Rocaglamide suppresses the activation of T cells and reduces naive CD4+ T cell differentiation into Th1/Th17 cells. Moreover, it decreases the secretion of IFN-γ and IL-17; thus, in turn, low-level expression of IFN-γ leads to lower cytotoxic mediators, lower activation of T cells, and lower differentiation of naive CD4+ T cells into the Th1 cells. A feedback loop then begins. However, the inhibition of p38 and JNK phosphorylation prevented rocaglamide-mediated decrease of NF-AT nuclear export.

(a)

(b)