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KMID : 0357920020360040238
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Korean Journal of Pathology
2002 Volume.36 No. 4 p.238 ~ p.242
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The Effect of Ischemic Preconditioning in Rat Liver: The Expression of Interleukin-1α and Nuclear Factor-ΚB
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Kum Yoon-Seup
Lee Soo-Kyoung
Kim Sun-Joo
Kwak Eun-Kyoung
Park Ji-Young
Park Tae-In
Bae Han-Ik
Sohn Yoon-Kyung
Suh In-Soo
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Abstract
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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.
Conclusion: 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.
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KEYWORD
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Reperfusion Injury, Ischemia, NF-Kappa B, Interleukin-1
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