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¹é¼­ °£ÀÇ Àç°ü·ù ¼Õ»ó¿¡¼­ ´Ü±â°£ ÇãÇ÷ÀüóġÀÇ È¿°ú : Interleukin-1¥á ¿Í Nuclear Factor- ¥ÊB ¹ßÇö The Effect of Ischemic Preconditioning in Rat Liver: The Expression of Interleukin-1¥á and Nuclear Factor-¥ÊB

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±ÝÀ±¼· ( Kum Yoon-Seup ) 
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À̼ö°æ ( Lee Soo-Kyoung ) 
°æºÏ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
±è¼±ÁÖ ( Kim Sun-Joo ) 
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°ûÀº°æ ( Kwak Eun-Kyoung ) 
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¹ÚÁö¿µ ( Park Ji-Young ) 
°æºÏ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
¹ÚÅÂÀΠ( Park Tae-In ) 
°æºÏ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
¹èÇÑÀÍ ( Bae Han-Ik ) 
°æºÏ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
¼ÕÀ±°æ ( Sohn Yoon-Kyung ) 
°æºÏ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç
¼­Àμö ( Suh In-Soo ) 
°æºÏ´ëÇб³ ÀÇ°ú´ëÇÐ º´¸®Çб³½Ç

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.

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.

Å°¿öµå

Reperfusion Injury;Ischemia;NF-Kappa B;Interleukin-1

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