Fig 1: Effects of G-Rh2 on AKT-Nrf2/NF-?Bp65 and p38-Nrf2/NF-?Bp65 signal pathways in IgE-sensitized RBL-2H3 cells. Protein levels were detected with Western blot. (A) Levels of p-AKT, AKT, p-p38, p38, Nrf2 and NF-?B. ##P < 0.01 vs. the Control group. *P < 0.05, **P < 0.01 vs. the IgE + Ag group. (B) Levels of p-AKT, AKT, Nrf2, Keap-1, p-p65, and NF-?B. ##P < 0.01 vs. the Control group. **P < 0.01 vs. the siControl + G-Rh2 group. (C) Levels of p-AKT, AKT, and Nrf2 (nuclear). ##P < 0.01 vs. the Control group. **P < 0.01 vs. the G-Rh2 group. (D) Levels of p-p38, p38, Nrf2, p-p65, and p65. ##P < 0.01 vs. the Control group. **P < 0.01 vs. the siControl + G-Rh2 group. (E) Levels of p-p38, p38, and Nrf2 (nuclear). #P < 0.05, ##p < 0.01 vs. the Control group. **P < 0.01 vs. the G-Rh2 group. Each data value represents the average value of 5 independent experiments (±SEM).
Fig 2: An illustration of the mechanism underlying the inhibitory effect of G-Rh2 on the FceRI signal pathway. G-Rh2 blocked IgE-induced mast cell degranulation by inhibiting AKT-Nrf2 and p38MAPK-Nrf2 signal pathways.
Supplier Page from Cell Signaling Technology for SignalSilence ® Akt1 siRNA I (Mouse Specific)