We have reported that triptolide can inhibit airway remodeling in a murine model of asthma via TGF-ß1/Smad signaling. In the present study, we aimed to investigate the effect of triptolide on airway smooth muscle cells (ASMCs) proliferation and the possible mechanism.
Triptolide significantly inhibited TGF-ß1-induced ASMC proliferation (P<0.05). The cell cycle was blocked at G1/S-interphase by triptolide dose dependently. No pro-apoptotic effects were detected under the concentration of triptolide we used. Western blottinganalysis showed TGF-ß1 induced Smad2 and Smad3 phosphorylation was inhibited by triptolide pretreatment, and the level of Smad7 was increased by triptolide pretreatment.
CONCLUSIONS:
Triptolide may function as an inhibitor of asthmaairway remodeling by suppressing ASMCs proliferation via negative regulation of Smad signaling pathway.