Inhibitory effect of salvianolic acid B on malondialdehyde-stimulated proliferation of rat hepatic stellate cells in vitro

2006 ◽  
Vol 14 (5) ◽  
pp. 476
Author(s):  
Xiao-Ling Wang ◽  
Ping Liu ◽  
Yun-Hua Cui ◽  
Xu-Dong Hu ◽  
Bo-Qin Li ◽  
...  
2006 ◽  
Vol 105 (1-2) ◽  
pp. 215-222 ◽  
Author(s):  
Yun-Lian Lin ◽  
Chia-Hung Wu ◽  
Miao-Hua Luo ◽  
Yeh-Jeng Huang ◽  
Chuen-Neu Wang ◽  
...  

2005 ◽  
Vol 60 (1-2) ◽  
pp. 139-142 ◽  
Author(s):  
Farid A. Badria ◽  
Abdel-Aziz A. Dawidar ◽  
Wael E. Houssen ◽  
Wayne T. Shier

There is a wealth of evidence that hepatic stellate cells (HSCs) orchestrate most of the important events in liver fibrogenesis. After liver injury, HSCs become activated to a profibrogenic myofibroblastic phenotype and can regulate net deposition of collagens and other matrix proteins in the liver. The proliferation of HSCs is mainly stimulated by the plateletderived growth factor (PDGF). In this study, some compounds from natural resources have been tested for their activity to inhibit PDGF-driven proliferative activity of rat HSCs. Apigenin, quercetin, genistein, daidzin, and biochanin A exhibited > 75% inhibitory activity against HSC-T6. It was found that, γ-linolenic (γ-Ln), eicosapentanoic (EPA) and α- linolenic (α-Ln) acids showed a high inhibitory effect on proliferation of rat HSCs at 50 nmol/l. Cholest-4-ene-3,6-dione and stigmastone-4-en-3,6-dione are the most active steroids with inhibitory activities > 80% and this is most likely due to the presence of the 4-en-3,6-dione moiety in both compounds. These results revealed that the compounds which effectively blocked HSC proliferation may be beneficial in liver fibrosis. Structure-activity relationships (SAR) may provide a basis for rational structure modification.


Gut ◽  
1999 ◽  
Vol 44 (1) ◽  
pp. 127-136 ◽  
Author(s):  
I Shimizu ◽  
Y Mizobuchi ◽  
M Yasuda ◽  
M Shiba ◽  
Y-R Ma ◽  
...  

BackgroundHepatic stellate cells play a key role in the pathogenesis of hepatic fibrosis.AimsTo examine the inhibitory effect of oestradiol on stellate cell activation.MethodsIn vivo, hepatic fibrosis was induced in rats by dimethylnitrosamine or pig serum. In vitro, rat stellate cells were activated by contact with plastic dishes resulting in their transformation into myofibroblast-like cells.ResultsIn the dimethylnitrosamine and pig serum models, treatment with oestradiol at gestation related doses resulted in a dose dependent suppression of hepatic fibrosis with restored content of hepatic retinyl palmitate, reduced collagen content, lower areas of stellate cells which express α smooth muscle actin (α-SMA) and desmin, and lower procollagen type I and III mRNA levels in the liver. In cultured stellate cells, oestradiol inhibited type I collagen production, α-SMA expression, and cell proliferation. These findings suggest that oestradiol is a potent inhibitor of stellate cell transformation.ConclusionThe antifibrogenic role of oestradiol in the liver may contribute to the sex associated differences in the progression from hepatic fibrosis to cirrhosis.


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