title: Effects of augmentation of liver regeneration recombinant plasmid on rat hepatic fibrosis.
abstract: OBJECTIVE
  To investigate the effects of eukaryotic expression of plasmid on augmentation of liver regeneration (ALR) in rat hepatic fibrosis and to explore their mechanisms.
  
  
  METHODS
  Ten rats were randomly selected from 50 Wistar rats as normal control group. The rest were administered intraperitoneally with porcine serum twice weekly. After 8 wk, they were randomly divided into: model control group, colchicine group (Col), first ALR group (ALR1), second ALR group (ALR2). Then colchicine ALR recombinant plasmid were used to treat them respectively. At the end of the 4th wk, rats were killed. Serum indicators were detected and histopathological changes were graded. Expression of type I, III, collagen and TIMP-1 were detected by immunohistochemistry and expression of TIMP-1 mRNA was detected by semi-quantified RT-PCR.
  
  
  RESULTS
  The histologic examination showed that the degree of the rat hepatic fibrosis in two ALR groups was lower than those in model control group. Compared with model group, ALR significantly reduced the serum levels of ALT, AST, HA, LN, PCIII and IV (P<0.05). Immunohistochemical staining showed that expression of type I, III, collagen and TIMP-1 in two ALR groups was ameliorated dramatically compared with model group (I collagen: 6.94+/-1.42, 5.80+/-1.66 and 10.83+/-3.58 in ALR1, ALR2 and model groups, respectively; III collagen: 7.18+/-1.95, 4.50+/-1.67 and 10.25+/-2.61, respectively; TIMP-1: 0.39+/-0.05, 0.20+/-0.06 and 0.53+/-0.12, respectively, P<0.05 or P<0.01). The expression level of TIMP-1 mRNA in the liver tissues was markedly decreased in two ALR groups compared with model group (TIMP-1 mRNA/beta-actin: 0.89+/-0.08, 0.65+/-0.11 and 1.36+/-0.11 in ALR1, ALR2 and model groups respectively, P<0.01).
  
  
  CONCLUSIONS
  ALR recombinant plasmid has beneficial effects on rat hepatic fibrosis by enhancing regeneration of injured liver cells and inhibiting TIMP-1 expressions.
authors.affiliation: Department of Epidemiology, Hebei Medical University, 361 Zhongshan Donglu, Shijiazhuang 050017, Hebei Province, China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Li
authors.forename: Dian-Wu
authors.initials: DW
authors.lastname: Liu
authors.forename: Li-Mei
authors.initials: LM
authors.lastname: Zhang
authors.forename: Bing
authors.initials: B
authors.lastname: Zhu
authors.forename: Yu-Tong
authors.initials: YT
authors.lastname: He
authors.forename: Yong-Hong
authors.initials: YH
authors.lastname: Xiao
mesh_terms: D000818:Animals; D024061:Collagen Type III / Q000378:metabolism; D015316:Genetic Therapy / Q000379:methods; D008103:Liver Cirrhosis / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D008115:Liver Regeneration / Q000502:physiology*; D008297:Male; D010957:Plasmids / Q000494:pharmacology*; D011506:Proteins / Q000235:genetics*; D051381:Rats; D017208:Rats, Wistar; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D050862:Oxidoreductases Acting on Sulfur Group Donors
chemical_list: D024061:Collagen Type III; D011506:Proteins; D019715:Tissue Inhibitor of Metalloproteinase-1; C088825:GFER protein, rat; D050862:Oxidoreductases Acting on Sulfur Group Donors