Mangifera indica L. extract (Vimang®) reduces plasma and liver cholesterol and leucocyte oxidative stress in hypercholesterolemic LDL receptor deficient mice.

Authors:
Gabriel G Dorighello
Gabriel G Dorighello
State University of Campinas
Brazil
Natalia M Inada
Natalia M Inada
São Carlos Institute of Physics
São Carlos | Brazil
Bruno A Paim
Bruno A Paim
State University of Campinas
Brazil
Anibal E Vercesi
Anibal E Vercesi
State University of Campinas
Brazil

Cell Biol Int 2018 Jun 1;42(6):747-753. Epub 2018 Mar 1.

Department of Structural and Functional Biology, Biology Institute, State University of Campinas, Campinas, São Paulo, Brazil.

Cardiovascular diseases are major causes of death worldwide. Beyond the classical cholesterol risk factor, other conditions such as oxidative stress are well documented to promote atherosclerosis. The Mangifera indica L. extract (Vimang®) was reported to present antioxidant and hypocholesterolemic properties. Thus, here we evaluate the effects of Vimang treatment on risk factors of the atherosclerosis prone model of familial hypercholesterolemia, the LDL receptor knockout mice. Mice were treated with Vimang during 2 weeks and were fed a cholesterol-enriched diet during the second week. The Vimang treated mice presented significantly reduced levels of plasma (15%) and liver (20%) cholesterol, increased plasma total antioxidant capacity (10%) and decreased reactive oxygen species (ROS) production by spleen mononuclear cells (50%), P < 0.05 for all. In spite of these benefits, the average size of aortic atherosclerotic lesions stablished in this short experimental period did not change significantly in Vimang treated mice. Therefore, in this study we demonstrated that Vimang has protective effects on systemic and tissue-specific risk factors, but it is not sufficient to promote a reduction in the initial steps of atherosclerosis development. In addition, we disclosed a new antioxidant target of Vimang, the spleen mononuclear cells that might be relevant for more advanced stages of atherosclerosis.

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Source
http://doi.wiley.com/10.1002/cbin.10950
Publisher Site
http://dx.doi.org/10.1002/cbin.10950DOI Listing

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June 2018
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