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Morphine Postconditioning Attenuates ICAM-1 Expression on Endothelial Cells

Authors
Min, Too JaeKim, Joong-ilKim, Jae-HwanNoh, Kyung HeeKim, Tae WooKim, Woon-YoungLee, Yoon-SookPark, Young Cheol
Issue Date
2월-2011
Publisher
KOREAN ACAD MEDICAL SCIENCES
Keywords
Morphine; Postconditioning; Reperfusion injury; Humans; Umblical Veins; Endothelial Cells; Cell Culture
Citation
JOURNAL OF KOREAN MEDICAL SCIENCE, v.26, no.2, pp.290 - 296
Indexed
SCIE
SCOPUS
KCI
Journal Title
JOURNAL OF KOREAN MEDICAL SCIENCE
Volume
26
Number
2
Start Page
290
End Page
296
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/113167
DOI
10.3346/jkms.2011.26.2.290
ISSN
1011-8934
Abstract
The purpose of this study is to determine 1) whether morphine postconditiong (MPostC) can attenuate the intercellular adhesion molecules-1 (ICAM-1) expression after reoxygenation injury and 2) the subtype(s) of the opioid receptors (ORs) that are involved with MPostC. Human umbilical vein endothelial cells (HUVECs) were subjected to 6 hr anoxia followed by 12 hr reoxygenation. Three morphine concentrations (0.3, 3, 30 mu M) were used to evaluate the protective effect of MPostC. We also investigated blockading the OR subtypes' effects on MPostC by using three antagonists (a mu-OR antagonist naloxone, a kappa-OR antagonist nor-binaltorphimine, and a delta-OR antagonist naltrindole) and the inhibitor of protein kinase C (PKC) chelerythrine. As results, the ICAM-1 expression was significantly reduced in the MPostC (3, 30 mu M) groups compared to the control group at 1, 6, 9, and 12 hours reoxygenation time. As a consequence, neutrophil adhesion was also decreased after MPostC. These effects were abolished by coadministering chelerythrine, nor-binaltorphimine or naltrindole, but not with naloxone. In conclusion, it is assumed that MPostC could attenuate the expression of ICAM-1 on endothelial cells during reoxygenation via the kappa and delta-OR (opioid receptor)-specific pathway, and this also involves a PKC-dependent pathway.
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