Evodiamine attenuates TGF-β1-induced fibroblast activation and endothelial to mesenchymal transition.

摘要: The aim of this study is to investigate the effect evodiamine on fibroblast activation in cardiac fibroblasts and endothelial mesenchymal transition (EndMT) human umbilical vein cells (HUVECs). Neonatal rat were stimulated with transforming growth factor beta 1 (TGF-β1) induce activation. After co-cultured (5, 10 μM), proliferation pro-fibrotic proteins expression evaluated. HUVECs also TGF-β1 EndMT treated 10 μM) at same time. response was evaluated as well capacity transitioned migrating surrounding tissue. As a result, Evodiamine-blunted induced into myofibroblast assessed by decreased expressions α-SMA. Furthermore, reduced increased protein fibrosis markers neonatal adult TGF-β1. exhibited lower levels CD31, CD34, higher α-SMA, vimentin than control cells. This phenotype eliminated both 5 10 μM evodiamine. Evodiamine significantly increase migration ability that occurred HUVECs. In addition, Smad2, Smad3, ERK1/2, Akt, nuclear translocation Smad4 HUVEC blocked treatment. Thus, could prevent from protect against EndMT. These effects may be mediated inhibition TGFβ pathway