In early atherogenesis, increased expression of surface cellular adhesion molecules
such as vascular cell adhesion molecule-1 (VCAM-1) and platelet endothelial cell adhesion
molecule-1 (PECAM-1) facilitates adhesion of monocytes to the endothelium and subsequent
monocyte infiltration into the intima. Therefore, the soluble form of cellular adhesion
molecules in plasma serves as important biomarker to predict cardiovascular risk factors.
Asiaticoside is an active compound derived from Centella asiatica (L.) and has been reported to possess anti-inflammatory and antipyretic effects [1].
The mechanism underlying anti-atherogenic effect of asiaticoside remains unknown.
This in vitro study aimed to evaluate the effect of asiaticoside on TNF-α-induced increased soluble
VCAM-1 (sVCAM-1) and soluble (sPECAM-1) levels as well as increased monocyte adhesion
and migration in human aortic endothelial cells (HAECs). HAECs were pretreated with
asiaticoside (6.25 – 50 µM) for 30 min followed by TNF-α stimulation (10 ng/mL) for
6h. The levels of sVCAM-1 and sPECAM-1 were measured by using FlowCytomix multiplex
kit purchased from eBioscience. Monocyte adhesion and migration assays were assessed
in static condition by co-incubating HAECs with fluorescently labeled monocytes. It
was shown that asiaticoside at the doses of 6.25, 12.5 and 25 µM significantly reduced
TNF-α-induced increased sPECAM-1 level by 62.3%, 92.3% and 61.3%, respectively (P< 0.05). However, all tested doses of asiaticoside failed to suppress the increased
sVCAM-1 level, increased monocyte adhesion and increased monocyte migration augmented
by TNF-α. Simvasatin (2 µM) was used as a positive control. Simvastatin inhibited
the sPECAM-1 level by 91.4% and the sVCAM-1 level by 60.2% (P< 0.05) but it failed to inhibit monocyte adhesion and migration elicited by TNF-α.
References:
[1] Wan J, Gong X, Jiang R, Zhang Z, Zhang L. Phytother Res 2013; 27: 1136 – 42
