[Role of nuclear factor-KappaB in endothelial injury in acute myocardial infarction].
OBJECTIVE
To examine the change in nuclear factor-KappaB (NF-KappaB) activity, tumor necrosis factor-alpha (TNF-alpha) and soluble thrombomodulin (sTM) levels at different time following reperfusion in acute myocardial infarction (AMI), and to identify the role of ischemia/reperfusion after ischemia in injury to endothelial cells and its relevant mechanism.


METHODS
AMI group included 8 randomly selected patients with AMI, and a normal control group (n=8) composing individuals who underwent health check. NF-KappaB activity in monocytes was determined by electrophoretic mobility shift assays (EMSA). The level of TNF-alpha was measured by radio-immunity and sTM was measured by enzyme linked immunosorbent assay (ELISA).


RESULTS
The NF-KappaB activity, TNF-alpha and sTM levels raised dramatically at 0.5 hour after reperfusion, reaching peak at 1 hour and declined gradually at 3, 12 and 24 hours. The levels of all the determined parameters at every time point were significantly higher than that of normal control group, and their levels at 1 hour were significantly higher than that at 24 hours (all P<0.05). There was a positive correlation between the NF-KappaB activity and the levels of TNF-alpha and sTM (all P<0.05).


CONCLUSIONS
These results indicate that NF-KappaB is activated and the levels of TNF-alpha and sTM rise significantly after reperfusion in AMI. The activation of NF-KappaB maybe one of the most important pathogenic mechanism of endothelial injury.
Liao
Xin-xue
XX
The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, Guangdong, China.
Li
Xin
X
Ma
Zhong-fu
ZF
Wang
Li-chun
LC
Du
Zhi-min
ZM
Dong
Yu-gang
YG
Ma
Hong
H
D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000473:pathology*; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D016328:NF-kappa B / Q000378:metabolism / Q000502:physiology*; D015912:Thrombolytic Therapy; D018180:Thrombomodulin / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D016328:NF-kappa B; D018180:Thrombomodulin; D014409:Tumor Necrosis Factor-alpha