title: Anti-fibrotic effect of plumbagin on CCl₄-lesioned rats.
abstract: OBJECTIVE
  Our previous studies have shown that plumbagin effectively inhibits hepatic stellate cell (HSC) proliferation. Thus, plumbagin-mediated anti-fibrotic effects in vivo merit further investigation.
  
  
  METHODS
  We used rat models to assess the potential benefits of plumbagin against CCl₄-induced liver fibrosis.
  
  
  RESULTS
  The results showed that plumbagin lowered the serum concentrations of liver functional enzymes (ALT, AST, ALB, TBIL) in CCl₄-fibrotic rats while reducing inflammatory cytokine levels (IL-6, TNF-α). As reflected in pathological examinations, rats that were administered plumbagin showed decreased collagen markers (HA, LN, PCIII and CIV) in liver tissues and improved hepatocellular impairments. In addition, plumbagin contributed to down-regulating NF-κB and TLR-4 mRNA in CCl₄-lesioned livers. As revealed in the immunohistochemical assay, plumbagin-administered rats showed reduced levels of α-SMA and TNF-α immunoreactive cells in liver tissue.
  
  
  CONCLUSIONS
  Collectively, these findings offer appealing evidence that plumbagin may serve as an anti-fibrotic medication through inactivating the NF-κB/TLR-4 pathway that is associated with inflammatory reactions, thereby mitigating liver fibrosis.
authors.affiliation: Department of Physiology, Faculty of Basic Medicine, Guangxi University of Chinese Medicine, Nanning, PR China.
authors.forename: Yanfei
authors.initials: Y
authors.lastname: Wei
authors.forename: Minkui
authors.initials: M
authors.lastname: Huang
authors.forename: Xuemei
authors.initials: X
authors.lastname: Liu
authors.forename: Zhang
authors.initials: Z
authors.lastname: Yuan
authors.forename: Yue
authors.initials: Y
authors.lastname: Peng
authors.forename: Zhenqing
authors.initials: Z
authors.lastname: Huang
authors.forename: Xuelin
authors.initials: X
authors.lastname: Duan
authors.forename: Tiejian
authors.initials: T
authors.lastname: Zhao
mesh_terms: D000199:Actins / Q000378:metabolism; D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002251:Carbon Tetrachloride / Q000633:toxicity; D003094:Collagen / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects; D005343:Fibrinolytic Agents / Q000494:pharmacology*; D015850:Interleukin-6 / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D009285:Naphthoquinones / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000199:Actins; D000410:Alanine Transaminase; D001219:Aspartate Aminotransferases; D002251:Carbon Tetrachloride; D003094:Collagen; D005343:Fibrinolytic Agents; D015850:Interleukin-6; D016328:NF-kappa B; D009285:Naphthoquinones; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; C498862:Acta2 protein, rat; C014758:plumbagin