Caracterización y cuantificación de células progenitoras endoteliales de ratas espontáneamente hipertensas alimentadas con fructosa
Objective: To examine alterations in participation of endothelial progenitor cells (EPC) because of insulin resistance (IR) associated with an experimental model of metabolic syndrome (MS) generated by chronic administration of fructose to spontaneously hypertensive rats (SHR) Material and metho...
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| Publicado en: | Revista Médica Universitaria |
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| Autores principales: | , , , , |
| Materias: | |
| Acceso en línea: | https://bdigital.uncu.edu.ar/fichas.php?idobjeto=3898 |
| Sumario: | Objective: To examine alterations in participation of endothelial progenitor cells (EPC)
because of insulin resistance (IR) associated with an experimental model of metabolic
syndrome (MS) generated by chronic administration of fructose to spontaneously
hypertensive rats (SHR)
Material and methods: WKY and SHR rats, male, were distributed into 4 groups (n = 8
c/u): WKY: control; FFR: WKY receiving fructose in drinking water to 10% (v/v) for 6
weeks , SHR; FFHR: SHR receiving fructose in drinking water to 10% (v/v) for
6 weeks. At the end of the protocol the following variables were determined: systolic
blood pressure, biochemical variables, HOMA index, levels of EPC quantified by flow
cytometry in peripheral blood and bone marrow, immunofluorescence in cell culture to
identify markers CD34 and VEGFR-2, EPC colony count and NAD(P)H-oxidase
activity in aortic tissue.
Results: We confirmed the experimental model based on metabolic variables
analyzed. A decrease in the levels of CPE, in peripheral blood and bone
marrow, which becomes more important groups of animals treated with fructose was
observed .In these groups there are also fewer colonies of developed EPC in cell
culture and exhibit an increased levels of oxidative stress, estimated by the activity
of NAD(P)H-oxidase.
Conclusion: the SM caused by chronic administration of fructose in FFHR has proven
to generate a decrease in the levels of CPE, as well as its functional capacity. The
intracellular mechanisms that produce this phenomenon could be triggered by the
degree of IR presented in this experimental model.
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