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Preconditioning and postconditioning reduce hepatic ischemia-reperfusion injury in rats.

AbstractBACKGROUND:
Ischemia-reperfusion injury occurs when ischemic tissues or organs suffer from further functional and structural damage when their blood supply recovers. This study aimed to contrast the protective effects of ischemic preconditioning and ischemic postconditioning in hepatic ischemia-reperfusion injury in rats.
METHODS:
Thirty-two healthy male Wistar rats were randomly divided into four groups: sham-operated (SO), ischemia-reperfusion (IR), ischemic preconditioning (I-pre), and ischemic postconditioning (I-post). Blood samples and hepatic tissue were taken from all groups after the experiments.
RESULTS:
There were significant differences between the IR, I-pre and I-post groups in alanine aminotransferase and aspartate aminotransferase levels, NF-kappaB p65 expression, apoptosis index and superoxide dismutase activity in hepatic tissue. There were no significant differences between the I-pre and I-post groups.
CONCLUSIONS:
Ischemic postconditioning and ischemic preconditioning reduce hepatic ischemia-reperfusion injury, but in clinical practice the former is a more appropriate choice.
AuthorsWan-Xing Zhang, Wen Yin, Lei Zhang, Lan-Hui Wang, Lei Bao, Hong-Fang Tuo, Li-Fang Zhou, Chun-Cheng Wang
JournalHepatobiliary & pancreatic diseases international : HBPD INT (Hepatobiliary Pancreat Dis Int) Vol. 8 Issue 6 Pg. 586-90 (Dec 2009) ISSN: 1499-3872 [Print] Singapore
PMID20007074 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Biomarkers
  • Rela protein, rat
  • Transcription Factor RelA
  • Superoxide Dismutase
  • Aspartate Aminotransferases
  • Alanine Transaminase
Topics
  • Alanine Transaminase (blood)
  • Animals
  • Apoptosis
  • Aspartate Aminotransferases (blood)
  • Biomarkers (blood)
  • Disease Models, Animal
  • Ischemic Preconditioning
  • Liver (blood supply, metabolism, ultrastructure)
  • Male
  • Rats
  • Rats, Wistar
  • Reperfusion Injury (metabolism, pathology, prevention & control)
  • Superoxide Dismutase (metabolism)
  • Transcription Factor RelA (metabolism)

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