| First Author | Park EJ | Year | 2012 |
| Journal | Biochem Pharmacol | Volume | 83 |
| Issue | 3 | Pages | 378-84 |
| PubMed ID | 22100726 | Mgi Jnum | J:181902 |
| Mgi Id | MGI:5314330 | Doi | 10.1016/j.bcp.2011.11.002 |
| Citation | Park EJ, et al. (2012) Schisandrin B suppresses TGFbeta1 signaling by inhibiting Smad2/3 and MAPK pathways. Biochem Pharmacol 83(3):378-84 |
| abstractText | TGFbeta1 plays a crucial role in the pathogenesis of vascular fibrotic diseases. Schisandra chinensis (S. chinensis), which is used as an oriental herbal medicine, is effective in the treatment of vascular injuries that cause aberrant TGFbeta1 signaling. In this study, we investigated whether S. chinensis extract and its active ingredients inhibit TGFbeta1 signaling in A7r5 vascular smooth muscle cells. We found that S. chinensis extract suppressed TGFbeta1 signaling via inhibition of Smad2/3 phosphorylation and nuclear translocation. Among the active ingredients of S. chinensis extract, schisandrin B (SchB) most potently inhibited TGFbeta1 signaling. SchB inhibited sustained phosphorylation and nuclear translocation of Smad2/3. Moreover, SchB suppressed TGFbeta1-induced phosphorylation of p38 and JNK, which contributed to Smad2/3 inactivation. The present study is the first to demonstrate that S. chinensis extract and SchB inhibit TGFbeta1 signaling. Our results may help future investigations to understand vascular fibrosis pathogenesis and to develop novel therapeutic strategies for treatment of vascular fibrotic diseases. |
