The Effect of Ischemic Preconditioning in Rat Liver: The Expression of Interleukin-1 and Nuclear Factor-B
Korean Journal of Pathology
; : 238-242, 2002.
Article
in Ko
| WPRIM
| ID: wpr-128464
Responsible library:
WPRO
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.
Key words
Full text:
1
Database:
WPRIM
Main subject:
RNA, Messenger
/
Reperfusion
/
Cell Survival
/
Polymerase Chain Reaction
/
Interleukin-1
/
Apoptosis
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Ischemic Preconditioning
/
In Situ Nick-End Labeling
/
Base Pairing
/
Hepatocytes
Limits:
Animals
Language:
Ko
Journal:
Korean Journal of Pathology
Year:
2002
Document type:
Article