AIM: It was the infectation of hepatovirus that results in hepatitis and hepatocirrhosis mainly. The primary objective of this study is to establish an animal model of hepatic fibrosis by the duck hepatitis B virus (D...
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AIM: It was the infectation of hepatovirus that results in hepatitis and hepatocirrhosis mainly. The primary objective of this study is to establish an animal model of hepatic fibrosis by the duck hepatitis B virus (DHBV) . METHODS: Each duckling born within 24 hours was injected with 0.1ml DHBV positive serum into vena cruralis once a week. From the 10th week,the dosage was increased to 0.2ml each time. Duck was killed after 16 *** indexes of hepatic fibrosis were assayed and the hepaticr histopathologyic changes and hepatocellular ultrastructure were observed. RESULTS: On hepaticr histopathological evaluation, the hepatic tissue of DHBV-induced model groups have hepatocellular oedema, fatty degeneration, inflammation and collagen deposition, which had no significant difference with the CCl4-induced model groups (P>0.05) . The level of serum type Ⅲ procollagen (PCⅢ) and serumal hyaluronic acid (HA) and hydroxyproline (Hyp) of hepatic tissue were increased significantly (P<0.01, P0.05, P0.01) . CONCLUSION The results showed that DHBV-induced duck model of hepatitis fibrosis is established successfully.
Objective:To study the effect of Salvia Miltirrhiza Bunge extraction (Salvianolic acid B) and Curcuma Longa Linn extraction (Curcumin) on the proliferation, activation and production of extracellular matrix in rat hep...
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Objective:To study the effect of Salvia Miltirrhiza Bunge extraction (Salvianolic acid B) and Curcuma Longa Linn extraction (Curcumin) on the proliferation, activation and production of extracellular matrix in rat hepatic stellate cells, and the relation between the effect and the extracellular signal regulated kinase expression level and its ***: The rat T6 hepatic stellate cells were cultured and treated by Salvianolic acid B or Curcumin according to the experimental protocols. The inhibition effect on the cell proliferation was determined by 3- (4, 5-dimthy-2-2thiazoly) 2, 5-dipheny-2H-tetrazoliun bromide colorimetry. The cells were harvested and lysed to extract the total cellular proteins. Proteins were separated by 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the expression levels of a smooth actin, type I collagen, and extracellular signal-regulated kinase after drug treatments were determined by Western ***: Salvianolic acid B and Curcumin inhibited the proliferation of rat hepatic stellate cells in dose-dependent fashion, reduced the expression level of α-smooth muscle actin significantly (P<0.01) . Curcumin reduced the expression of type I collagen significantly (P0.05) . Both of Salvianolic acid B and Curcumin had no significant effect on the expression level of extracellular signal-regulated kinase, but could significantly down-regulate phosphorylated extracellular signal-regulated kinase expression level (P0.05 vs. P0.01, respectively) .Conclusion: Salvianolic acid B and Curcumin could significantly inhibit the proliferation, activation and production of extracellular matrix in rat hepatic stellate cells, and the effect was associated with the reduction of phosphorylated extracellular signal regulated kinase 1/2 expression level. The drug or drug compound with multi-effect-pathways and multi-effect-targets may have better anti-hepatic fibrosis effect than a single drug alone.
Objective: We constructed an oligonucleotide microarray with 50 probes representing 50 hepatic fibrosis-associated genes. We substituted the HSC-T6 cells for original hepatic stellate cells, aimed to investigate the e...
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Objective: We constructed an oligonucleotide microarray with 50 probes representing 50 hepatic fibrosis-associated genes. We substituted the HSC-T6 cells for original hepatic stellate cells, aimed to investigate the effects of 4 different components of EZHU (curcuma aramatica oil,curcumol,β-elemence,Curcumin) on the gene expression in cultured activated hepatic stellate cells, and explored the molecular mechanism of anti-hepatic fibrosis for EZHU at gene network level. Methods: We looked up the mRNA sequence of 50 liver fibrosis-related genes such as TGFβ1, PDGF, IL-6, IL-10, HGF, ICAM-1, MIP-2, TGFβRI, TGFβR Ⅱ,PDGFRα,PDGFRβ,TNFαR1,MMP2,TIMP1 from the gene bank,designed oligonucleotide probes by software of designing oligonucleotide *** synthesized oligonucleotides in PE8909DNA synthesizing instrument, and made out oligonucleotide microarray with OGR-04 droping instrument and aldehyded glass chip. Cultured HSC-T6 cells were treated with different concentrations of medicines (colchicine, curcuma aramatica oil,curcumol, β-elemence,curcumin) .According to the experiment of cells toxicity,we took the appropriate concentrations of medicines whose cells livability was higher than 50% as experiment concentrations. We setted up the blank comparison each team in the same time, and gathered the cells at 4 point of 1h, 6h, 12h, 24h, *** distilled total RNA with Trizol reagent according to the operation process,then labeled cDNAs from total RNA with cy3-dUTP and *** labeled cDNAs were hybrided to an oligonucleotide microarray, then we washed the oligonucleotide microarray a few times. Afterwards, we scanned the gene microarray by scanner Genepix 4000B, and analysed the difference of gene expression of HSC-T6 cells with ImaGene 4.2 ***: After HSC-T6 cells were cultured in medium with 6.25μg/ml of colchicine for 12h, gene expression of TIMP-1 was down-regulated 2.2 bolds,TIMP-2 and IL-6 were down-regulated 2.3, 2.0 bolds, respectively, aft
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