title: Hepatoprotective effects of baicalein against CCl₄-induced acute liver injury in mice.
abstract: OBJECTIVE
  To investigate the hepatoprotective effect of baicalein against carbon tetrachloride (CCl₄)-induced liver damage in mice.
  
  
  METHODS
  Mice were orally administered with baicalein after CCl₄ injection, and therapeutic baicalein was given twice a day for 4 d. The anti-inflammation effects of baicalein were assessed directly by hepatic histology and serum alanine aminotranferease and aspartate aminotransferase measurement. Proliferating cell nuclear antigen was used to evaluate the effect of baicalein in promoting hepatocyte proliferation. Serum interleukin (IL)-6, IL-1β and tumor necrosis factor-α (TNF-α) levels were measured by enzyme-linked immunosorbent assay and liver IL-6, TNF-α, transforming growth factor-α (TGF-α), hepatocyte growth factor (HGF) and epidermal growth factor (EGF) genes expression were determined by quantitative real-time polymerase chain reaction.
  
  
  RESULTS
  CCl₄-induced acute liver failure model offers a survival benefit in baicalein-treated mice. The data indicated that the mRNA levels of IL-6 and TNF-α significantly increased within 12 h after CCl₄ treatment in baicalein administration groups, but at 24, 48 and 72 h, the expression of IL-6 and TNF-α was kept at lower levels compared with the control. The expression of TGF-α, HGF and EGF was enhanced dramatically in baicalein administration group at 12, 24, 48 and 72 h. Furthermore, we found that baicalein significantly elevated the serum level of TNF-α and IL-6 at the early phase, which indicated that baicalein could facilitate the initiating events in liver regeneration.
  
  
  CONCLUSIONS
  Baicalein may be a therapeutic candidate for acute liver injury. Baicalein accelerates liver regeneration by regulating TNF-α and IL-6 mediated pathways.
authors.affiliation: Laboratory of Regenerative Medicine, Department of Hepatobiliary Surgery, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, Guangdong Province, China.
authors.forename: Hai-Li
authors.initials: HL
authors.lastname: Huang
authors.forename: Ya-Jing
authors.initials: YJ
authors.lastname: Wang
authors.forename: Qing-Yu
authors.initials: QY
authors.lastname: Zhang
authors.forename: Bin
authors.initials: B
authors.lastname: Liu
authors.forename: Fang-Yuan
authors.initials: FY
authors.lastname: Wang
authors.forename: Jing-Jing
authors.initials: JJ
authors.lastname: Li
authors.forename: Run-Zhi
authors.initials: RZ
authors.lastname: Zhu
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001219:Aspartate Aminotransferases / Q000378:metabolism; D002251:Carbon Tetrachloride / Q000633:toxicity*; D049109:Cell Proliferation; D044950:Flavanones / Q000494:pharmacology*; D022781:Hepatocytes / Q000166:cytology; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008099:Liver / Q000293:injuries* / Q000378:metabolism; D017114:Liver Failure, Acute / Q000139:chemically induced* / Q000188:drug therapy*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D044950:Flavanones; D053583:Interleukin-1beta; D015850:Interleukin-6; D018809:Proliferating Cell Nuclear Antigen; D014409:Tumor Necrosis Factor-alpha; C006680:baicalein; D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase