title: [Protecting effects of p44/42 MAPK signal transduction pathway on hepatocytes in ischemic preconditioning].
abstract: OBJECTIVE
  To investigate the significance of PKC and p44/42 mitogen-activated protein kinase (MAPK) signal transduction in ischemic preconditioning (IP).
  
  
  METHODS
  Through liver cell IP models, PKC inhibitor and MEK inhibitor were utilized to analyze the phosphorylation level of p44/42 MAPK and cell viability was also observed. Rat liver IP models were established which were treated with various drugs. Then the phosphorylation level of p44/42 MAPK in vivo and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) concentrations were detected. And cellular structures were observed under light microscopy.
  
  
  RESULTS
  Similar results were obtained in vivo and in vitro IP models. Compared with the ischemia reperfusion (IR) group in vivo, the phosphorylation level of p44/42 MAPK was obviously increased in IP treated rats (q = 27.217, P < 0.01), and the cellular structure injured slightly. The concentrations of serum ALT and AST in IP group were significantly lower than those in IR group (281.0 U/L +/-35.6 U/L vs 762.8 U/L +/-130.5 U/L and 407.7 U/L +/-73.7 U/L vs 820.9 U/L +/-111.3 U/L, P < 0.01). However, opposite changes were found in PKC and MEK inhibited groups, when compared to IP group. The phosphorylation level of p44/42 MAPK was obviously decreased, the liver tissues injured evidently, and the concentrations of serum ALT and AST (645.61 U/L +/-90.4 U/L, 678.6 U/L +/-136.5U/L and 466.2 U/L +/-82.8 U/L, 732.9 U/L +/-91.1 U/L, respectively) were significantly greater than those in IP group.
  
  
  CONCLUSIONS
  These results suggest that p44/42 MAPK pathway plays a vital role in the protection of hepatocytes in ischemic preconditioning.
authors.affiliation: Department of Organ Transplantation Surgery, Zhujiang Hospital, First Military Medical University, Guangzhou 510280, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Gao
authors.forename: Yu
authors.initials: Y
authors.lastname: Wang
authors.forename: Ming-xin
authors.initials: MX
authors.lastname: Pan
authors.forename: Er-wei
authors.initials: EW
authors.lastname: Sun
authors.forename: Yu-qiang
authors.initials: YQ
authors.lastname: Shan
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D022781:Hepatocytes / Q000166:cytology / Q000502:physiology; D006801:Humans; D019194:Ischemic Preconditioning; D008099:Liver / Q000098:blood supply* / Q000166:cytology; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D010766:Phosphorylation; D011493:Protein Kinase C / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction
chemical_list: D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D011493:Protein Kinase C; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3