[Liposomal form of lipoic acid: preparation and determination of antiplatelet and antioxidant activity].

Autor: Shchelkonogov VA; Moscow technological University (MITHT), Moscow, Russia., Sorokoumova GM; Moscow technological University (MITHT), Moscow, Russia., Baranova OA; Pirogov Russian National Research Medical University (RNRMU), Moscow, Russia., Chekanov AV; Pirogov Russian National Research Medical University (RNRMU), Moscow, Russia., Klochkova AV; Pirogov Russian National Research Medical University (RNRMU), Moscow, Russia., Kazarinov KD; Kotelnikov Institute of Radioengineering and Electronics, (Fryasino branch), Fryazino, Moscow region, Russia., Solovieva EY; Pirogov Russian National Research Medical University (RNRMU), Moscow, Russia., Fedin AI; Pirogov Russian National Research Medical University (RNRMU), Moscow, Russia., Shvets VI; Moscow technological University (MITHT), Moscow, Russia.
Jazyk: ruština
Zdroj: Biomeditsinskaia khimiia [Biomed Khim] 2016 Jul; Vol. 62 (5), pp. 577-583.
DOI: 10.18097/PBMC20166205577
Abstrakt: Optimal conditions for obtaining phosphatidylholine (PC) liposomes with lipoic acid (LA) are chosen that lead to the formation of nanoparticles with a size of 175¸284 nm with efficiency (extent) of inclusion of LA in liposomes equal 85% and characterized by a slow release of substance from the nanoparticles. The effect of "empty" liposomes and liposomal form of LA on platelet aggregation induced by arachidonic acid (AA) is established. It is found that liposomes with LА inhibit platelet aggregation, caused by AА, to 80%. In addition, it is shown that "empty" liposomes slightly (to 30%) suppress platelet aggregation, caused by AА. The amount of TBA-sensitive products in samples of platelet-rich plasma (PRP) incubated with liposomal LA is determined. It is shown that LA in the composition of liposomes retains its antioxidant properties, and the amount of products of lipid peroxidation in platelet-rich plasma decreases in a dose-dependent manner when arachidonic acid is used as an inductor of platelet aggregation. It is assumed that the antiplatelet action of the liposomal form of LА is induced by inhibition of the initiation of lipid peroxidation products caused by exogenous inducer AА. It is supposed that, after additional research, the liposomal form of LA can be considered as a new drug in complex treatment of cerebral ischemia.
Databáze: MEDLINE