Impact of salvianolic acid-B on TGF-beta1-induced HK-2 epithelial-mesenchymal transition.
- Author:
	        		
		        		
		        		
			        		Juan ZHOU
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Fei WANG
			        		
			        		;
		        		
		        		
		        		
			        		Haiying LU
			        		
			        		;
		        		
		        		
		        		
			        		Yue ZHANG
			        		
			        		
		        		
		        		
		        		
			        		
			        		Author Information
			        		
 - Publication Type:Journal Article
 - MeSH: Benzofurans; pharmacology; Bone Morphogenetic Protein 7; pharmacology; Cadherins; metabolism; Cell Differentiation; drug effects; Cell Line; Epithelial Cells; pathology; Humans; Mesoderm; pathology; Transforming Growth Factor beta1; pharmacology
 - From: China Journal of Chinese Materia Medica 2010;35(1):89-93
 - CountryChina
 - Language:Chinese
 - 
		        	Abstract:
			       	
			       		
				        
				        	
OBJECTIVETo investigate the effect of salvianolic-acid B (SA-B) on epithelia-mesenchymal transition in human renal proximal tubular cells (HK2), induced by transforming growth factor beta1 (TGF-beta1).
METHODEpithelia-mesenchymal transition (EMT) was induced with TGF-beta1 in HK2 cultured in vitro. Different concentrations (2, 5, 10, 20 microg x L(-1)) and stimulant periods (12, 24, 48 h) were tried to find the perfect condition for EMT. At the same time bone morphogenetic protein-7 (BMP-7, positive control) and the SA-B intervention were given to observe their effect on EMT. Western blot and immunofluorescent microscopy were used to analyze the expression of E-cadherin and alpha-smooth muscle actin (alpha-SMA) in HK2.
RESULTBMP-7 significantly inhibited the down-regulation of E-cadherin and the up-regulation of alpha-SMA induced by TGF-beta1 (P < 0.05), and SA-B significantly inhibited the up-regulation of alpha-SMA expression induced by TGF-beta1 (P < 0.05), but not the down-regulation of E-cadherin induced by TGF-beta1.
CONCLUSIONSA-B and BMP-7 can inhibit TGF-beta1-induced EMT in HK2. Their common role is to inhibit the up-regulation of alpha-SMA, and the effect of SA-B on the regulation of E-cadherin needs further study to be confirmed.
 
            