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Background and Purpose: liver fibrosis is liver repair response on a variety of chronic liver injury, mainly for liver extracellular matrix synthesis and degradation imbalance, resulting in excessive deposition of extracellular matrix. Fibronectin (Fibronectin, FN) is an important component of the extracellular matrix. The study showed that the the liver fibrosis early FN content that increase. Hepatic stellate cells (HSC) is the key to the pathological changes of liver fibrosis, the study was designed by dimethylnitrosamine (DMN) model of hepatic fibrosis observation FN and its receptor in hepatic fibrosis process changes explore salvianolic acid B (SA-B) on the inhibition of hepatic fibrosis. Method: 1, the in vivo experiments: 30 of Wistar male rats were randomly divided into normal group, model group and SA-B treatment group, normal diet, with free access to water. Model group and SA-B group once DMN 10μg · kg-1, 2 Tian intraperitoneal injection for 4 weeks, 14 induced rat liver fibrosis. SA-B in the beginning of the modeling 10mg/kg orally, normal and model groups irrigation with normal saline for 4 weeks, all rats were sacrificed in model 4 weekend. Serum alanine aminotransferase enzyme (ALT), aspartate aminotransferase (AST), and total bilirubin (TBil) and albumin (Alb) level. HE staining to observe pathological changes of rat liver inflammation; hydrochloric acid hydrolysis method for the determination of liver tissue hydroxyproline (Hyp) content, immunohistochemistry and Western blot analysis of α-smooth muscle actin (alpha-SMA), integrin α5β1 and FN expression. The gelatin zymography Determination liver tissue MMP-2, MMP-9 activity. Vitro: recovery of HSC-T6 cell lines, 10% FBS / DMEM subculture divided into normal group, and FN packet group and sub-4h, 8h, 12h, 24h, 36h observation point. Select to generation HSC-T6 pharmacodynamic experiments are divided into four groups: normal group, model group, SA-B group (final concentration 10-6 mol / L ,10-5 mol / L). Model group and SA-B group are FN package to be normal and model groups plus 0.5% fetal calf serum (FCS), SA-B group and 0.5? S SA-B. MTT and alamarBlue Determination of HSC proliferation. The immunofluorescence observed α-SMA, integrin α5β1 protein expression. Western blot analysis of α-SMA, integrin α5β1 protein expression. Results: 1, compared with the normal group, model group weight was significantly reduced, liver / body mass index was significantly lower (p lt; 0.01); compared with the model group, body weight and liver / body mass index of SA-B rats elevated (p lt; 0.01). Compared with the normal group, model group, liver tissue central vein and portal area fiber interval formation and collagen deposition significantly, liver tissue Hyp content increased (p-lt; 0.01), the expression of α-SMA and FN and α5β1 protein increased (p-values ??are lt; 0.01), MMP-2, MMP-9's activity increased (p lt; 0.01). SA-B after administration of rat liver hyperplasia fiber thin collagen deposition, The Hyp content compared with the model group to reduce (p lt; 0.01), α-SMA and FN and α5β1 protein expression of decline (p value lt; 0.01), MMP-2 MMP-9 activity weakened (p = lt; 0.01, lt; 0.05), the difference was significant. 2, the serum was significantly promote the proliferation of HSC-T6 uncoated FN group. The FN package is significantly promote the proliferation of HSC-T6 and α-SMA expression. The FN package is significantly promote early HSC-T6 adherent, stretching, proliferation, α-SMA and α5β1 expression, SA-B inhibition of FN stimulation of HSC-T6 proliferation and α-SMA and α5β1 expression. Conclusion: SA-B can significantly reduce the inflammation and necrosis of liver cells, reduce collagen deposition in the liver, inhibit the development of liver fibrosis. One of the mechanisms of SA-B antifibrotic to inhibit liver α5β1 receptor expression to inhibit FN conjunction reducing excessive extracellular matrix deposition.
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