Does salvianolic acid B prevent epithelial-to-mesenchymal transition through the TGF-beta1 signal transduction pathway in vivo and in vitro?
Sal B can prevent tubular EMT in the fibrotic kidney induced by HgCl2 as well as HK-2 cells triggered by TGF-beta1, the mechanism of Sal B is closely related to the regulation of TGF-beta1/Smads pathway, manifested as the inhibition of TGF-beta1 expression, suppression of TbetaR-I expression and function, down-regulation of Smad2/3 phosphorylation, and restoration of the down-regulation of Smad7, as well as inhibition of MMP-2 activity.
ILK expression does not appear to have a role in predicting outcome in patients with resected HCC.