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Conclusions: Asiatic acid improves TNF-a-stimulated endothelial barrier im- that IFN-γ induced upregulation of ICAM-1 expression, which was started at 8h,
pairment. This is associated with inhibition of cytoskeletal rearrangement and coinciding with downregulation of VCAM-1 expression. However, PECAM-1 ex-
VCAM-1 expression induced by TNF-a. Furthermore, asiatic acid also suppresses pression remained unaltered.
the production of sICAM-1 and sVCAM-1, which are soluble biomarkers com-
Conclusions: IFN--induced endothelial dysfunction may be closely related to
monly used to assess endothelial function and to predict the risk of future cardio-
the impairment of barrier integrity, reduced NO bioavailability and altered cell
vascular events. These data support the use of asiatic acid as a potential therapeu-
phenotypes. These findings enrich the current knowledge on the mechanisms of
tic agent against TNF--induced endothelial dysfunction.
IFN- in disrupting the endothelial function.