title: [OMT inhibited TGF-β1-induced cardiac fibroblast proliferation via down-regulating p38MAPK phosphorylation in vitro].
abstract: OBJECTIVE
  To investigate the inhibitory effects of OMT on TGF-β1-induced CFBs proliferation, and then explore the mechanism.
  
  
  METHODS
  The experiment was randomly divided into 6 groups as following: control group (serum free DMEM), model group (20 μg x L(-1) TGF-β1), OMT low dose group (1.89 x 10(-4) mol x L(-1) + 20 μg x L(-1) TGF-β1), OMT medium dose group (3.78 x 10(-4) mol x L(-1) + 20 μg x L(-1) TGF-β1), OMT high dose group (7.56 x 10(-4) mol x L(-1) + 20 μg x L(-1) TGF-β1), SB203580 group (p38MAPK blocking agent, 1 x 10(-5) mol x L(-1) + 20 μg x L(-1) TGF-β1). Vimentin of CFBs was identified by immunocytochemical methods, α-SMA of myFBs as well. Inhibitory effects of OMT on CFBs proliferation was detected by the MTT assay. Picric acid Sirius red staining was analyzed collagen type I and collagen type III deposition. Western blot was determined the expression of p38MAPK, p-p38MAPK, collagen type I and collagen type III.
  
  
  RESULTS
  MTT results showed that OMT significantly inhibited CFBs proliferation induced by TGF-β1 (P < 0.01) α-SMA immunocytochemical experiments suggested that OMT could protect against the CFBs proliferation. OMT could significantly decrease the deposition of collagen type I and collagen type III by Western bloting and picric acid Sirius red staining. Western blot results showed that TGF-β1 enhanced p38MAPK phosphorylation, however OMT attenuated the phosphorylation of p38MAPK induced by TGF-β1 (P < 0.01).
  
  
  CONCLUSIONS
  OMT can inhibit the CFBs proliferation induced by TGF-β1, and its mechanism may be involved in inhibiting p38MAPK phosphorylation.
authors.forename: Hai
authors.initials: H
authors.lastname: Xiao
authors.forename: Yi-ni
authors.initials: YN
authors.lastname: Xu
authors.forename: Hong
authors.initials: H
authors.lastname: Luo
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Yan-yan
authors.initials: YY
authors.lastname: Zhang
authors.forename: Ling
authors.initials: L
authors.lastname: Tao
authors.forename: Yan
authors.initials: Y
authors.lastname: Jiang
authors.forename: Xiang-chun
authors.initials: XC
authors.lastname: Shen
mesh_terms: D000470:Alkaloids / Q000494:pharmacology*; D000818:Animals; D049109:Cell Proliferation / Q000187:drug effects; D003094:Collagen / Q000378:metabolism; D015536:Down-Regulation; D005260:Female; D005347:Fibroblasts / Q000187:drug effects; D006321:Heart / Q000187:drug effects*; D066298:In Vitro Techniques; D008297:Male; D010766:Phosphorylation; D011807:Quinolizines / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D053773:Transforming Growth Factor beta1 / Q000037:antagonists & inhibitors*; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000093842:Matrines
chemical_list: D000470:Alkaloids; D003094:Collagen; D011807:Quinolizines; D053773:Transforming Growth Factor beta1; D048051:p38 Mitogen-Activated Protein Kinases; C037573:oxymatrine; D000093842:Matrines