Id |
Subject |
Object |
Predicate |
Lexical cue |
S1 |
0-113 |
Sentence |
denotes |
Aspirin inhibits nuclear factor-kappa B mobilization and monocyte adhesion in stimulated human endothelial cells. |
S2 |
114-330 |
Sentence |
denotes |
BACKGROUND: The induction of vascular cell adhesion molecule-1 (VCAM-1) and E-selectin by tumor necrosis factor-alpha (TNF) is mediated by mobilization of the transcription factor nuclear factor-kappa B (NF-kappa B). |
S3 |
331-590 |
Sentence |
denotes |
Since salicylates have been reported to inhibit NF-kappa B activation by preventing the degradation of its inhibitor I kappa B, we studied a potential inhibition of this pathway by acetylsalicylate (aspirin) in human umbilical vein endothelial cells (HUVECs). |
S4 |
591-766 |
Sentence |
denotes |
METHODS AND RESULTS: Gel-shift analyses demonstrated dose-dependent inhibition of TNF-induced NF-kappa B mobilization by aspirin at concentrations ranging from 1 to 10 mmol/L. |
S5 |
767-971 |
Sentence |
denotes |
Induction of VCAM-1 and E-selectin surface expression by TNF was dose-dependently reduced by aspirin over the same range, while induction of intercellular adhesion molecule-1 (ICAM-1) was hardly affected. |
S6 |
972-1090 |
Sentence |
denotes |
Aspirin appeared to prevent VCAM-1 transcription, since it dose-dependently inhibited induction of VCAM-1 mRNA by TNF. |
S7 |
1091-1261 |
Sentence |
denotes |
As a functional consequence, adhesion of U937 monocytes to TNF-stimulated HUVECs was markedly reduced by aspirin due to suppression of VCAM-1 and E-selectin upregulation. |
S8 |
1262-1385 |
Sentence |
denotes |
These effects of aspirin were not related to the inhibition of cyclooxygenase activity, since indomethacin was ineffective. |
S9 |
1386-1649 |
Sentence |
denotes |
CONCLUSIONS: Our data suggest that aspirin inhibits NF-kappa B mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin. |