Fig. 7: Tetrandrine and DIM inhibited the activation of Syk-PLCγ2 signaling pathway through AhR.

a RAW264.7 cells were transfected with either siAhR, and followed by treatment with tetrandrine (0.3āμM) for 6āh, and then exposed to RANKL (100āng/mL) for 15āmin. The levels of p-Syk, Syk, p-PLCγ2 and PLCγ2 were evaluated by western blots. b BMMs were treated with tetrandrine (0.3āμM) for 6āh in the presence or absence of CH223191 (3āμM), and followed with RANKL (100āng/mL) for 15āmin. The levels of p-Syk, Syk, p-PLCγ2 and PLCγ2 were evaluated by western blots. c, d BMMs were treated with tetrandrine (0.3āμM) or DIM (10āμM) for 6āh in the presence or absence of CH223191 (3āμM), and followed with RANKL (100āng/mL) for 40āmin. The localization of NFATc1 was visualized by western blots and immunofluorescence analysis. Results are expressed as the meansā±āS.E.M. from at least 3 independent experiments. *Pā<ā0.05, **Pā<ā0.01 vs. indicated group. siAhR: AhR siRNA. siCtrl: control siRNA