title: Experimental evidence for the protective effects of coffee against liver fibrosis in SD rats.
abstract: BACKGROUND
  Coffee is one of the most commonly consumed beverages worldwide. Accumulating clinical evidence has shown an inverse relationship between coffee and liver cirrhosis. We investigated the protective effect of coffee against liver fibrosis and underlying molecular mechanisms using a dimethylnitrosamine (DMN)-induced liver fibrosis model.
  
  
  RESULTS
  Coffee administration significantly prevented the deterioration of body weight, organ weight, and serum biochemistry by DMN treatment. Histopathological examination revealed that necrosis/inflammation and fibrotic septa decreased significantly in coffee-treated rats compared to those treated with DMN and water. Coffee administration also significantly inhibited the accumulation of hydroxyproline (P < 0.001) and the production of malondialdehyde (P < 0.05), as well as stellate cell activation caused by DMN injection. Coffee protected the depletion of glutathione, superoxide dismutase, and catalase in liver tissue. In addition, coffee treatment inhibited the gene expression of inducible nitric oxide synthase, transforming growth factor (TGF)-beta, tumor necrosis factor-alpha, interleukin-1, and platelet-derived growth factor (PDGF)-beta in liver tissues, and lowered the concentration of TGF-beta and PDGF-beta in liver. Coffee inhibited NO production by macrophages.
  
  
  CONCLUSIONS
  Coffee exerts protective effects against liver fibrosis via antioxidant action and the suppression of fibrogenic cytokines, TGF-beta and PDGF-beta.
authors.affiliation: East-West Immune Center, Institute of Traditional Medicine and Bioscience of Daejeon University, Daejeon 301-724, Republic of Korea.
authors.forename: Jang-Woo
authors.initials: JW
authors.lastname: Shin
authors.forename: Jing-Hua
authors.initials: JH
authors.lastname: Wang
authors.forename: Jong-Koo
authors.initials: JK
authors.lastname: Kang
authors.forename: Chang-Gue
authors.initials: CG
authors.lastname: Son
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001835:Body Weight / Q000187:drug effects; D040503:Coffea; D003069:Coffee; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004128:Dimethylnitrosamine; D004195:Disease Models, Animal; D015870:Gene Expression; D055166:Hepatic Stellate Cells / Q000187:drug effects; D006909:Hydroxyproline / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D008103:Liver Cirrhosis / Q000139:chemically induced / Q000188:drug therapy*; D008264:Macrophages / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009336:Necrosis / Q000517:prevention & control; D009569:Nitric Oxide / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D010982:Platelet-Derived Growth Factor / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012639:Seeds
chemical_list: D000975:Antioxidants; D003069:Coffee; D016207:Cytokines; D010936:Plant Extracts; D010982:Platelet-Derived Growth Factor; D009569:Nitric Oxide; D008315:Malondialdehyde; D052247:Nitric Oxide Synthase Type II; D004128:Dimethylnitrosamine; D006909:Hydroxyproline