Enhanced inhibition of platelet aggregation in-vitro by niosome-encapsulated indomethacin.

In order to achieve sustained antiplatelet effect from indomethacin, it was incorporated in a non-ionic surfactant vesicle (niosome). The objective was to study the effect of niosomal-encapsulated indomethacin on platelet function such as inhibition of aggregation and ATP release induced by a variety of agonists (adenosine 5'-diphosphate (ADP), epinephrine, arachidonic acid, ristocetine) and to explore the feasibility of carrier-mediated drug delivery to the platelets. Multilamellar vesicles (niosomes) were prepared from Tween-60 by the lipid hydration method. Freshly prepared human platelet rich plasma (PRP) was used for aggregation/inhibition studies, the extent of which was observed as a change in light transmission measured by the Chronolog Aggregometer. The percent inhibition of aggregation induced by the agonist ADP ranged from 28. 21+/-0.28 at the 2.0 micromol level to 92.6+/-1.20 at 12.7 micromol of the encapsulated drug while the same concentrations of the drug inhibited aggregation only to the extent of 13.75+/-0.13 and 36. 82+/-0.57%, respectively. A 100% inhibition of aggregation induced by arachidonic acid was achieved by niosomal indomethacin while inhibition by the free drug was 41.9% at equimolar concentrations. ATP release study showed that 100% inhibition was achieved by 8 micromol of the encapsulated drug while inhibition by the free drug was 40.00+/-1.82%. Therefore, at equimolar doses, the niosomal drug proved to be more efficient in inhibiting platelet aggregation than the free drug, probably due to greater quantity of the drug reaching the specific site of inhibition in the interior of the platelets and acting directly on the cyclo-oxygenase system to prevent thromboxane formation.