title: [Mechanism of oxymatrine in preventing hepatic fibrosis formation in patients with chronic hepatitis B].
abstract: OBJECTIVE
  To explore the mechanism of oxymatrine in preventing hepatic fibrosis formation in patients with chronic hepatitis B (CHB).
  
  
  METHODS
  A total of 80 CHB patients receiving routine therapies for liver protection and support were divided into two groups. Oxymatrine at the daily dose of 150 mg was injected intravenously in the therapeutic group (n=40), and gluthion (1.2 g daily) was injected in the control group (n=40) for 8 weeks. The liver functions, indexes of hepatic fibrosis and the levels of transforming growth factor-beta1 (TGF-beta1), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) were measured in these patients before and after the therapy.
  
  
  RESULTS
  Liver functions was obviously improved after therapy in both groups, showing no significant difference between them (P>0.05). The indexes of hepatic fibrosis such as HA, LN, PCIII and C-IV were significantly lower in the therapeutic group than in the control group (P<0.01). The serum levels of TGF-beta1 and TNF-alpha decreased while IL-10 increased significantly after the treatment in the therapeutic group (P<0.05).
  
  
  CONCLUSIONS
  The effect of oxymatrine against hepatic fibrosis is mediated by lowering the levels of TGF-beta1 and TNF-alpha and increasing the level of IL-10 in CHB patients.
authors.affiliation: Department of Infectious Diseases, First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China. dr.jxliang@126.com
authors.forename: Jian-xin
authors.initials: JX
authors.lastname: Liang
authors.forename: Xing-fen
authors.initials: XF
authors.lastname: Qu
authors.forename: Wen-ting
authors.initials: WT
authors.lastname: Zeng
authors.forename: Ke-lun
authors.initials: KL
authors.lastname: Zhu
authors.forename: He
authors.initials: H
authors.lastname: Zhang
authors.forename: Jian-jun
authors.initials: JJ
authors.lastname: Wei
mesh_terms: D000328:Adult; D000470:Alkaloids / Q000627:therapeutic use*; D005260:Female; D019694:Hepatitis B, Chronic / Q000188:drug therapy* / Q000473:pathology; D006801:Humans; D016753:Interleukin-10 / Q000097:blood; D008103:Liver Cirrhosis / Q000188:drug therapy / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008875:Middle Aged; D011807:Quinolizines / Q000627:therapeutic use*; D053773:Transforming Growth Factor beta1 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D000093842:Matrines
chemical_list: D000470:Alkaloids; D016753:Interleukin-10; D011807:Quinolizines; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; C508609:IL10 protein, human; C508960:TGFB1 protein, human; C037573:oxymatrine; D000093842:Matrines