Objective To explore the relationships and significance among the tissue inhibitor of metalloproteinases-1(TIMP-1), hyaluronia acid(HA), procollagen type Ⅲ(PCⅢ), procollagen type Ⅳ(CⅣ) and laminin(LN) in the serum of hepatitis patients.
Objective To investigate the clinical significance of the changes of serun procollagen typeⅢ (PCⅢ) and transforming growth factor betal (TGF-β 1) levels in patients with hepatolenticular degeneration (HLD).
Further, Vit E diminished the increased collagen content [(0.23±0.01) vs (0.60±0.11), P<0.05] and inhibited the increased α1 (I) procollagen mRNA expression [(0.28±0.01) vs (0.85±0.15), P<0.05] in the liver in model group.
Type Ⅰ procollagen mRNA expression and MDA contents were significantly decreased respectively (5.2±1.4 vs 3.8±1.1,P<0.05 and 12.7±2.6 vs 8.2±2.0mmol/g, P<0.05), however, the MMPs activities were not changed.
同时观察到Lu使肝脏Ⅰ型前胶原mRNA表达降低(5.2±1.4 vs 3.8±1.1,P<0.05)和MDA含量显著减少(12.7±2.6 vs 8.2±2.0μmmol/g,P<0.05),但MMPs的活性没有改变。
The expression of TGFβ 1 protein in liver tissues were detected by immunohistochemical methods in 45 cases with viral hepatitis and cirrhosis,and the serum level of TGFβ 1,hyaluronic acid (HA),laminin(LN),collagen type Ⅳ(Ⅳ-C) and precollagen type Ⅲ(PⅢP)were measured in 21 of these 45 cases.
Objective: To examine the hepatic fibrosis serum marker levels of Laminin (LN), Precollagen typeⅢ (pcⅢ), Collagen type Ⅳ (CⅣ) and Hyalurohic acid (HA) in different clinical types of hepatitis and other liver and gall diseases and so as to explore their clinical value in diagnosis.
Objective The rat model with immune liver fibrosis was established to study the effect of composite formula-Ganxianyu Formula on the levels of serum laminin(LN),hyaluronic acid(HA), precollagen typeⅢ(PCⅢ)and hydroxyproline(Hyp)in the liver and to investigate the mechanism of Ganxianyu Formula for anti-fibrosis in the liver.
Methods Effects of platelet derived growth factor (PDGF) and calcium antagonist, verapamil (Ver), on collagen biosynthesis, expression of procollagen types Ⅰ and Ⅲ mRNA of HC were investigated by in situ hybridization and 3H Proline incorporation.
In recent studies the qualification for this purpose of enzymes such as procollagen prolyl hydroxylase and lysosomal N-Acetyl-β-glucosaminidase and the N-terminal peptide of procollagen type III has been tested.
Study of serum procollagen type III peptide in patients with hepatic cirrhosis from a clinical point of view
In the course of CVB3 myocarditis, CTGF upregulation coincided with increased cardiac TGF-β and procollagen type I mRNA expression, preceding the formation of fibrotic lesions.
The significantly enhanced transcript levels of TGF-β, CTGF, and procollagen type I in cultivated CVB3-infected primary cardiac fibroblasts substantiate the role of fibroblasts as a relevant cell population in cardiac remodeling processes.
Additionally, serum procollagen type III (PIIINP) levels and hepatic collagenase activity were measured to determine hepatic collagen synthesis and degradation.
The dynamics of total protein and procollagen biosynthesis was studied in the muscle tissue in gunshot wound during the natural healing and after treatment with antioxidant (AO) 2,6-di-tert-butyl-4-methylphenol (BHT).
AO treatment considerably decreased the rate of both total protein and procollagen synthesis in the muscle on the third day of healing.
Immunocytochemistry showed no changes in morphology or staining patterns for type-I procollagen, type-II collagen, keratan sulfate and unsulfated chondroitin.
Targeted inhibition of type I procollagen synthesis by antisense DNA oligonucleotides
Antisense DNA oligonucleotides directed against specific sequences within α1(I) and α2(I) mRNA of type I procollagen were complexed to a cell-specific carrier, and screened for their effectiveness in reducing α1(I) and α2(I) mRNA levels.
Heterogeneity of liver cells expressing procollagen types I and IV in vivo
Northern analysis revealed that FSC and UMSC expressed identical patterns of mRNAs for IGF-I and transforming growth factor (TGF) -β2, for osteopontin, and for procollagen Types I and III (Type I>amp;gt;Type III).
The detection of the mRNAs of procollagen types I, II and III in human fetal fingers by in situ hybridization using digoxigenin-
Bone morphogenetic protein-1 cleaves the C-terminal propeptides of procollagen types I, II, and III.