The Effect of Ischemic Preconditioning in Rat Liver: The Expression of Interleukin-1 and Nuclear Factor-B.
- Author:
Kum Yoon SEUP
1
;
Soo Kyoung LEE
;
Sun zoo KIM
;
Eun Kyoung KWAK
;
Ji Young PARK
;
Tae In PARK
;
Han Ik BAE
;
Yoon Kyung SOHN
;
In Soo SUH
Author Information
1. Department of Pathology, Kyungpook University School of Medicine, Daegu, Korea. issuh@knu.ac.kr
- Publication Type:Original Article
- Keywords:
Reperfusion Injury-Ischemia-NF-kappa B-Interleukin-1
- MeSH:
Animals;
Apoptosis;
Base Pairing;
Cell Survival;
Endothelial Cells;
Hepatocytes;
In Situ Nick-End Labeling;
Interleukin-1*;
Ischemia;
Ischemic Preconditioning*;
Liver*;
Polymerase Chain Reaction;
Rats*;
Reperfusion;
RNA, Messenger
- From:Korean Journal of Pathology
2002;36(4):238-242
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: A short period of ischemia and reperfusion, called ischemic preconditioning, protects various tissues against subsequent sustained ischemic insult. Apoptosis of hepatocytes and sinusoidal endothelial cells are a critical mechanisms of injury in the ischemic liver. Because nuclear factor-B (NF-B) has a significant role in the cell survival, we hypothesized that ischemic preconditioning protects by inhibition of apoptosis through the expression of NF-B, induced by interleukin-1 (IL-1), which is known for enhancement of its transcription and activation. METHODS: We induced ischemia and reperfusion on rat liver, and performed in situ terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labelling assay and polymerase chain reaction for IL-1 mRNA and NF-B mRNA. RESULTS: Apoptosis of hepatocytes and sinusoidal endothelial cells, assessed by in situ TUNEL assay, was significantly reduced with preconditioning. The expression of IL-1 mRNA and NF-B mRNA are seen on discrete monoclonal bands around 344 and 356 base pairs, in comparison with normal rat liver, but, there was no significant difference between the ischemia-reperfusion group and the preconditioning group. CONCLUSIONS: We suggest that ischemic preconditioning confers dramatic protection against prolonged ischemia via inhibition of apotosis through the expression of IL-1 inducing NF-B and its activation. However, we need further study in the activity of NF-B, such as nucleotide shift assay, because the activity of NF-B is regulated by binding of the inhibitory protein, IB.
