Enoxaparin reduced monocyte adhesion and the expression of ICAM-1 and P-selectin in human endothelial cells exposed to hydrogen peroxide, demonstrating its antioxidant effect.
Does enoxaparin reduce oxidative stress-induced activation in cultured human endothelial cells?
Enoxaparin exerts antioxidant and anti-inflammatory effects on human endothelial cells by reducing monocyte adhesion and modulating cell adhesion molecules and nuclear transcription factors.
There are data that document the anti-inflammatory effect of enoxaparin (EP) and its possible antioxidant potential. This study was designed to search for the antioxidant mechanism(s) of EP directly on endothelial cells exposed to an oxidant stimulus. For this purpose cultured human endothelial cells were exposed to nontoxic concentrations of hydrogen peroxide in the presence or absence of EP, and the adhesion of monocytes, the expression of cell adhesion molecules and transcription factors possibly involved in the process were tested. Adhesion assays, ELISA and Western blot analysis revealed that EP reduced monocyte adhesion, ICAM-1 and P-selectin expression, decreased the nuclear levels of c-Jun and p65 proteins, and diminished the phosphorylation of c-Jun protein, MAPK p38 and JNK. Together, the data demonstrate the antioxidant effect of EP and the involvement of ICAM-1, P-selectin, MAPK p38, JNK and the transcription factors NF-kappaB and AP-1 in the mechanism of action of this drug.
Mânduțeanu et al. (Mon,) conducted a other in H2O2-induced activation of human endothelial cells. Enoxaparin vs. Absence of enoxaparin was evaluated on Monocyte adhesion, expression of cell adhesion molecules (ICAM-1, P-selectin), and transcription factors. Enoxaparin reduced monocyte adhesion and the expression of ICAM-1 and P-selectin in human endothelial cells exposed to hydrogen peroxide, demonstrating its antioxidant effect.