Qinggan Huoxue Recipe suppresses epithelial-to-mesenchymal transition in alcoholic liver fibrosis through TGF-β1/Smad signaling pathway

Figure 6 Potential mechanism underlying Qinggan Huoxue Recipe-mediated inhibition of epithelial-to-mesenchymal transition in alcoholic liver fibrosis rats. TGF-β1 stimulates responsive cells through binding and activating the transmembrane receptors TGF-β type I (TGF-βR-I) and type II (TGF-βR-II). Receptor ternary complexes phosphorylate and activate Smad2/3. Once activated, Smad2/3 forms heterocomplexes with Smad4, and these translocate to the nucleus and activate TGF-β1 signaling. Snail, a gene associated with the TGF-β/Smad signaling pathway, inhibits E-cadherin expression, increases vimentin and fibronectin levels, promotes EMT and decreases the levels of occludin, ZO-1 and claudin. QGR, HXR and QGHXR suppressed the effects of ALF-induced modulation of the TGF-β/Smad signaling pathway and ameliorated EMT-induced alcoholic fibrosis. QGR, HXR and QGHXR affected molecules associated with the TGF-β/Smad signaling pathway in the same manner. However, QGR and HXR exerted no significant changes in vimentin mRNA expression, QGR exerted no significant changes in fibronectin mRNA expression, and HXR exerted no significant changes in Snail and TGF-β1 mRNA expression.