title: Caffeine protects against alcoholic liver injury by attenuating inflammatory response and oxidative stress.
abstract: OBJECTIVE
  The present investigation was designed to determine the effects of caffeine on alcohol-induced hepatic injury in mice.
  
  
  METHODS
  Five groups of mice (8 each) were used.
  
  
  METHODS
  The mice treated with different doses of caffeine (5, 10, and 20 mg/kg, respectively).
  
  
  METHODS
  The degree of alcoholic liver injury was evaluated biochemically by measuring serum markers and pathological examination. Real time PCR and ELISA methods were used to check the expression of cytokines and CYP 450.
  
  
  RESULTS
  Treatment with caffeine significantly attenuated the elevated serum aminotransferase enzymes and reduced the severe extent of hepatic cell damage, steatosis and the immigration of inflammatory cells. Interestingly, caffeine decreased hepatic mRNA expression of lipogenic genes, while it had no effect on protein expression of hepatic CYP2E1. Furthermore, caffeine decreased serum and tissue inflammatory cytokines levels, tissue lipid peroxidation and inhibited the necrosis of hepatocytes. Kupffer cells isolated from ethanol-fed mice produced high amounts of reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF-alpha), whereas Kupffer cells from caffeine treatment mice produced less ROS and TNF-alpha.
  
  
  CONCLUSIONS
  These findings suggest that caffeine may represent a novel, protective strategy against alcoholic liver injury by attenuating oxidative stress and inflammatory response.
authors.affiliation: School of Pharmacy, Anhui Medical University, Shushan District, Hefei, China.
authors.forename: Xiongwen
authors.initials: X
authors.lastname: Lv
authors.forename: Zhen
authors.initials: Z
authors.lastname: Chen
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Hongfeng
authors.initials: H
authors.lastname: Liu
authors.forename: Cheng
authors.initials: C
authors.lastname: Huang
authors.forename: Pengli
authors.initials: P
authors.lastname: Zhu
mesh_terms: D000818:Animals; D002110:Caffeine / Q000494:pharmacology*; D002478:Cells, Cultured; D000697:Central Nervous System Stimulants / Q000494:pharmacology*; D018925:Chemokines / Q000378:metabolism; D019392:Cytochrome P-450 CYP2E1 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D000431:Ethanol / Q000494:pharmacology; D007249:Inflammation / Q000378:metabolism*; D007728:Kupffer Cells / Q000166:cytology / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000697:Central Nervous System Stimulants; D018925:Chemokines; D016207:Cytokines; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D002110:Caffeine; D000431:Ethanol; D008315:Malondialdehyde; D019392:Cytochrome P-450 CYP2E1