[Emodin inhibits the proliferation and migration of human pulmonary artery smooth muscle cells by blocking SMAD2/3 signaling pathway].

Objective To investigate the effect of emodin on the proliferation and migration of human pulmonary artery smooth muscle cells (HPASMCs) induced by transforming growth factor β1 (TGF-β1). Methods HPASMCs were cultured in vitro, and HPASMCs in logarithmic growth phase were divided into control group, TGF-β1 group, and TGF-β1 combined with emodin group. The activity of HPASMCs was detected by CCK-8 assay, the migration ability of HPASMCs was detected by Transwell chamber assay and scratch assay, and the expressions of osteopontin (OPN) and proliferating cell nuclear antigen (PCNA) were detected by immunofluorescence assay. The protein levels of OPN and PCNA and the phosphorylation of SMAD family member 2 (SMAD2) and SMAD family member 2 (SMAD3) in HPASMCs were detected by Western blot. Results Compared with those in the control group, in TGF-β1 group, the protein expressions of OPN and PCNA, the proliferation and migration of HPASMCs, and the phosphorylation of SMAD2 and SMAD3 were increased. Compared with those in the TGF-β1 group, in the TGF-β1 combined with emodin group, the proliferation and migration of HPASMCs, the expressions of OPN and PCNA, and the phosphorylation of SMAD2 and SMAD3 were decreased. Conclusion Emodin inhibits the up-regulation of OPN and PCNA and the proliferation and migration of PASMCs induced by TGF-β1, which may be related to the blocking of SMAD2/3 signaling pathway.