Depression of Macrophages Modifies Serum Lipid Profile in Hyperlipidemia


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Suppression of functional activity of macrophages by gadolinium chloride, suppressing the macrophage population and the endocytosis velocity, was studied in vivo. Injection of GdCl3 led to an increase in serum cholesterol concentration. Preliminary injection of GdCl3 to mice with lipidemia 24 h before poloxamer 407 reduced the concentrations of triglycerides and LDL during marked depression of macrophages (in 24 h). Macrophage repopulation (days 5, 7) was associated with development of a trend to an increase of triglyceride and LDL levels. lectron microscopic study of Kupffer cells after injection of poloxamer 407 and its combination with gadoliniun chloride detected the intralysosomal accumulation syndrome in these cells (formation of auto- and heterophagolysosomes). Activity of cathepsin B, characteristic of macrophages, reduced 24 h after injections of GdCl3 and poloxamer 407 alone and restored in response to their combination.

Sobre autores

N. Goncharova

Institute of Physiology and Basic Medicine

Autor responsável pela correspondência
Email: pathol@inbox.ru
Rússia, Novosibirsk

A. Pupyshev

Novosibirsk State Medical University, Ministry of Health of the Russian Federation

Email: pathol@inbox.ru
Rússia, Novosibirsk

E. Filyushina

Institute of Physiology and Basic Medicine

Email: pathol@inbox.ru
Rússia, Novosibirsk

K. Loktev

Institute of Physiology and Basic Medicine

Email: pathol@inbox.ru
Rússia, Novosibirsk

E. Korolenko

University Canada West

Email: pathol@inbox.ru
Canadá, Vancouver

E. Lushnikova

Institute of Molecular Pathology and Pathomorphology

Email: pathol@inbox.ru
Rússia, Novosibirsk

O. Molodykh

Institute of Molecular Pathology and Pathomorphology

Email: pathol@inbox.ru
Rússia, Novosibirsk

T. Korolenko

Institute of Physiology and Basic Medicine

Email: pathol@inbox.ru
Rússia, Novosibirsk

B. Churin

Institute of Molecular Pathology and Pathomorphology

Email: pathol@inbox.ru
Rússia, Novosibirsk


Declaração de direitos autorais © Springer Science+Business Media New York, 2016

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