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

Figure 6

Rocaglamide treatment changes the cytokine expression of allograft recipients, affects the immune response ability of T cells to the same identical gene tissues, and suppresses the nuclear expression of NF-AT, but not that of BF-Kb. (a–d) The levels of IL-6 (a), IL-4 (b), IL-10 (c), and TGF-β (d) in the serum and supernatants curve from MLR were detected by using commercially available ELISA kits. Each reaction was conducted in triplicate (, , and ). (e) To investigate the effectiveness of rocagalmide on the proliferation of T cells, both in the spleen and lymph nodes, and we performed mixed lymphocyte reaction assays. Data from three separate wells were dedicated to each responder-stimulator, and each experiment was repeated thrice (; , , and ). (f) T cell activation induced by the nuclear expression of NF-AT was downregulated. Jurkat T cells were stimulated with PMA and ionomycin for 2 h with or without rocaglamides (added 1 h before stimulation). Nuclear proteins were extracted and immunoblotted with mAb against NFATc1. (g) The nuclear proteins were immunoblotted with Abs to p65. (h) Rocaglamides activate MAPKs, p38, and JNK. Jurkat T cells were stimulated with PMA and ionomycin for 2 h in the absence or presence of various concentrations of rocaglamides (added 1 h before stimulation). Total cell lysates were immunoblotted with Abs against phosphorylated p38 (p-p38) and phosphorylated JNK.

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