title: [Effects of cordyceps acid and cordycepin on the inflammatory and fibrogenic response of hepatic stellate cells].
abstract: OBJECTIVE
  To investigate the effects of cordyceps acid and cordycepin on the inflammatory phenotype and fibrogenic property of hepatic stellate cells (HSCs).
  
  
  METHODS
  An immortalized mouse HSC line (JS1) was stimulated with lippolysaccharide (LPS; 100 ng/ml) to induce an inflammatory response with or without co-administration of cordyceps acid or cordycepin in various concentrations (10, 50, or 200 mumol/L). Effects of the treatments on the chemokine monocyte chemotactic protein-1 (MCP-1) mRNA expression in the cells and the protein secretion in the cell culture supernatants were determined by reverse transcription and real-time quantitative PCR (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. In addition, JS1 cells were treated with transforming growth factor-b1 (TGFb1; 10 ng/ml) to induce a fibrogenic response with or without co-administration of cordyceps acid or cordycepin in various concentrations (10, 50, or 200 mumol/L). Effects on the expression of fibrogenic proteins including collagen type I and a-smooth muscle actin (a-SMA), were investigated by Western blot.
  
  
  RESULTS
  High-concentration (200 mumol/L) treatments of both cordyceps acid and cordycepin significantly inhibited the LPS-induced up-regulation of MCP-1 transcription and secretion (mRNA: 2.07 +/- 0.29 vs. 3.35 +/- 0.26, t = 15.90 and 1.15 +/- 0.23 vs. 4.17 +/- 0.61, t = 8.93; protein: 1.88 +/- 0.06 vs. 2.33 +/- 0.06, t = 10.39 and 1.47 +/- 0.25 vs. 1.97 +/- 0.04, t = 4.60; all P less than 0.05). All concentrations of cordyceps acid and cordycepin inhibited the TGFb1-induced up-regulation of collagen type I and a-SMA protein expression. However, the effects were more robust with the 200 mumol/L concentrations (P less than 0.05).
  
  
  CONCLUSIONS
  Cordyceps acid and cordycepin ameliorate the LPS-induced inflammatory phenotype and TGFb1-induced fibrogenic response of cultured HSCs. These effects may contribute significantly to the drugs' therapeutic mechanisms to inhibit and resolve liver fibrosis.
authors.affiliation: Zhongshan Hospital, Fudan University, Shanghai 200032, China.
authors.forename: Yang-Yang
authors.initials: YY
authors.lastname: Ouyang
authors.forename: Zhe
authors.initials: Z
authors.lastname: Zhang
authors.forename: Yi-Rong
authors.initials: YR
authors.lastname: Cao
authors.forename: Yuan-Qing
authors.initials: YQ
authors.lastname: Zhang
authors.forename: Yan-Yan
authors.initials: YY
authors.lastname: Tao
authors.forename: Cheng-Hai
authors.initials: CH
authors.lastname: Liu
authors.forename: Lie-Ming
authors.initials: LM
authors.lastname: Xu
authors.forename: Jin-Sheng
authors.initials: JS
authors.lastname: Guo
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D032661:Cordyceps; D055166:Hepatic Stellate Cells / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D018932:Chemokine CCL2; D053773:Transforming Growth Factor beta1