ghd hair Recombinant human augmenter of liver rege

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Recombinant human augmenter of liver regeneration on hepatic fibrosis tissue inhibitor of metalloproteinase gene expression of -1

Each time each group were killed six living,[link widoczny dla zalogowanych], cut the same part of the liver, in addition to pathological left,[link widoczny dla zalogowanych], the other immersed into liquid nitrogen, then stored into a 70 ℃. 3. Immune human serum albumin liver injury model: reference WANG Bao-en, etc. Methods immune human serum albumin liver injury model. 130 Wistar rats by the method of modeling. Survival after mold removal 87. Grouped as follows: model group 18,[link widoczny dla zalogowanych], negative control group 23 (model after intraperitoneal injection of normal saline), hALR low dose group 23 (model 1Ottg/kg day after I hALR weight intraperitoneally). hALR high-dose group 23 (model hALR day after to 50 ~ g / kg body weight intraperitoneally); 18 weeks of age with normal rats as normal control group. 5 After the model animals, hA-LR for 1 month, hALR for 2 months each of 3 time points each were killed 6 living, cut the same part of the liver, in addition to pathological examination to stay,[link widoczny dla zalogowanych], the rest rapidly into liquid nitrogen, then stored into a 70 ℃. 4 liver extraction of total RNA, cDNA synthesis, amplified quantitative PCR, quantitative analysis of amplified products: See our previous methods have been reported. 5. Statistical analysis: results are mean ± standard deviation of (± s) that the application of single-factor analysis of variance. Results 1. hALR of CCI4 toxicity of liver fibrosis in the gene expression of TIMP1 in Table 1. Table 1hALR of CC1, toxic liver fibrosis TIMP1 gene expression (± 5) Note: with the touch reorganization and negative control group, P <0012. hALR on albumin immunological liver injury in rats TIMPl gene expression in Table 2. * 53 Table 2hALR on albumin immunological liver injury in rats TllCiY '~ _-based solid expression of tj ± 5) Note: The model group and the negative control group. . P <0.01 for the discussion of liver extracellular matrix (EcM) due to excessive accumulation. Various pathogenic factors through direct or indirect role in promoting the synthesis of ECM. Result in the fibrous connective tissue between the portal area and hepatic lobule hyperplasia, the formation of liver fibrosis. Recent studies suggest that hepatic fibrosis and liver metabolism of ECM synthesis and degradation related to metabolic imbalance. The synthesis of ECM including collagen, noncollagenous glycoproteins and proteoglycans; enzymes involved in the metabolism of ECM degradation is mainly matrix metalloproteinases (MMPs); tissue inhibitor of metalloproteinases (TIMPs) is a specific inhibitor of MMPs, by inhibiting the activity of MMPs in liver fibrosis, play an important role in the development of l. We use carbon tetrachloride toxicity and albumin in the two kinds of immune injury of the liver fibrosis model has been formed hALR on rat liver fibrosis of a tissue inhibitor of metalloproteinase 1 (TIMP1) gene expression, the results show that Low doses of the two models in the treatment of liver tissue hALR TIMP1 gene expression levels in different stages of the treatment process and the model was no significant difference between groups; high dose group hALR TIMP1 gene expression in liver tissue were significantly lower than model group. This suggests that there is inhibition of hepatic fibrosis hALR TIMP1 gene expression. By inhibiting the expression of TIMP1 gene, thus contributing to the degradation of ECM may be reversed hALR one of the mechanisms of liver fibrosis.

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