Effect of pterostilbene complexed with cyclodextrin on rat liver: potential reduction of oxidative damage and modulation redox-sensitive proteins

The objectives of this study were to promote the aqueous solubility of pterostilbene (PTS) by complexation with hydroxypropyl-β-cyclodextrin (HPβCD), characterize the complex under physical aspects, to make its oral administration feasible in biological tests, and to investigate their pharmacologica...

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Published in:Medicinal chemistry research Vol. 27; no. 10; pp. 2265 - 2278
Main Authors: Lacerda, Denise S., Bianchi, Sara E., Pinós, Wesley L., Campos-Carraro, Cristina, Türck, Patrick, Hickmann, Alexandre R., Pittol, Vanessa, Teixeira, Rayane B., Belló-Klein, Adriane, Bassani, Valquiria L., Araujo, Alex S. R.
Format: Journal Article
Language:English
Published: New York Springer US 01-10-2018
Springer Nature B.V
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Summary:The objectives of this study were to promote the aqueous solubility of pterostilbene (PTS) by complexation with hydroxypropyl-β-cyclodextrin (HPβCD), characterize the complex under physical aspects, to make its oral administration feasible in biological tests, and to investigate their pharmacological properties. For 14 days, rats received daily PTS:HPΒCD complex at doses of 25, 50, or 100 mg kg −1 per day orally. The results showed no kidney or liver damage, nor any induction of apoptosis by the administered doses. Also, the complex showed dose-dependent antioxidant effects in the rat liver, as evidenced by a reduction in lipid peroxidation and reactive oxygen species, as well as an increase in non-enzymatic antioxidant. PTS:HPΒCD complex also increased the expression of sensitive redox proteins such as AKT and GSK-3β related to the insulin signaling pathway in the liver. Thus, the complexation demonstrated to be able to increase the apparent solubility of PTS making feasible dose curve administration and could be a food alternative complementary to antioxidant therapeutic. Therefore, the PTS:HPβCD complex can be used for prevention of diseases related to oxidative damage and insulin signaling.
ISSN:1054-2523
1554-8120
DOI:10.1007/s00044-018-2233-6