title: Antifibrotic effects of protocatechuic aldehyde on experimental liver fibrosis.
abstract: BACKGROUND
  Recent studies have demonstrated that transforming growth factor-β1 (TGF-β1) and connective transforming growth factor (CTGF) are associated with the pathophysiology of liver fibrosis. We isolated protocatechuic aldehyde, the major degradation of phenolic acids.
  
  
  OBJECTIVE
  This study was carried out to investigate the potential antifibrotic effect of Protocatechuic aldehyde (PA) on experimental liver fibrosis in vitro and in vivo, and to explore its possible mechanism.
  
  
  METHODS
  Cell proliferation was determined. Type I collagen, type III collagen, transforming growth factor-β1 (TGF-β1) and connective transforming growth factor (CTGF) were measured by ELISA kits in TNF-α stimulated HSCs. In the carbon tetrachloride (CCL(4))-induced rat liver fibrosis model, liver fibrosis grade and histopathological changes were evaluated, and biochemical indicators were determined. Furthermore, immunostaining and Western blot analysis were used to detect hepatic TGF-β1 and CTGF expression in liver tissue.
  
  
  RESULTS
  Overall, our results indicated that PA inhibits HSCs proliferation, inhibits the levels of TGF-β1, CTGF, type I collagen and type III collagen in TNF-α stimulated HSCs. Treatment of PA causes a significant reduction in fibrosis grade, ameliorates biochemical indicators and histopathological morphology, and reduces liver TGF-β1 and CTGF expression in rat model of CCL(4)-induced liver fibrosis.
  
  
  CONCLUSIONS
  These findings suggest that PA has potentially conferring antifibrogenic effects.
authors: School of pharmacy, Yantai University, PR China.
authors: Chunmei
authors: C
authors: Li
authors: Wanglin
authors: W
authors: Jiang
authors: Haibo
authors: H
authors: Zhu
authors: Jian
authors: J
authors: Hou
mesh_terms: D000818:Animals; D001547:Benzaldehydes / Q000494:pharmacology*; D015153:Blotting, Western; D002251:Carbon Tetrachloride; D002396:Catechols / Q000494:pharmacology*; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D055513:Connective Tissue Growth Factor / Q000378:metabolism; D019610:Cytoprotection; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D055166:Hepatic Stellate Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006820:Hyaluronic Acid / Q000378:metabolism; D007150:Immunohistochemistry; D007797:Laminin / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008103:Liver Cirrhosis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D001547:Benzaldehydes; C526316:CCN2 protein, rat; D002396:Catechols; D024042:Collagen Type I; D024061:Collagen Type III; D007797:Laminin; D020011:Protective Agents; C508962:Tgfb1 protein, rat; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D055513:Connective Tissue Growth Factor; C005581:protocatechualdehyde; D006820:Hyaluronic Acid; D002251:Carbon Tetrachloride