Next Article in Journal
Cell Fate Control by Translation: mRNA Translation Initiation as a Therapeutic Target for Cancer Development and Stem Cell Fate Control
Next Article in Special Issue
7-O-Methylpunctatin, a Novel Homoisoflavonoid, Inhibits Phenotypic Switch of Human Arteriolar Smooth Muscle Cells
Previous Article in Journal
Mechanism of Action and Interactions between Thyroid Peroxidase and Lipoxygenase Inhibitors Derived from Plant Sources
Previous Article in Special Issue
Emerging Role of Vitamin D and its Associated Molecules in Pathways Related to Pathogenesis of Thrombosis
Open AccessArticle

Development of a Predictive Model to Induce Atherogenesis and Hepato-Renal Impairment in Female Rats

1
Laboratory of Electrophysiology and Cardiovascular Pharmacology, Faculty of Health Sciences, Federal University of Grande Dourados (UFGD), Dourados, MS 79825-070, Brazil
2
Laboratory of Preclinical Research of Natural Products, Paranaense University (UNIPAR), Umuarama, PR 87502-210, Brazil
*
Author to whom correspondence should be addressed.
Biomolecules 2019, 9(11), 664; https://doi.org/10.3390/biom9110664
Received: 27 August 2019 / Revised: 17 September 2019 / Accepted: 20 September 2019 / Published: 29 October 2019
Therapeutic approaches for the treatment of dyslipidemia and atherosclerosis have radically changed in recent decades. Part of this advance undeniably stems from basic biomedical research that has provided a better understanding and identification of new therapeutic targets. The aim of this work was to develop a model to induce atherogenesis and hepato-renal impairment in female Wistar rats. The following groups received the respective treatments for 60 days: control animals, non-ovariectomized rats that received an atherogenic diet (NEAD), ovariectomized rats that received an atherogenic diet (NOAD), non-ovariectomized rats that received an atherogenic diet and oral Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME; LEAD), and ovariectomized rats that received an atherogenic diet and oral l-NAME (LOAD). Animals in the NEAD, NOAD, LEAD, and LOAD groups also received methimazole and cholecalciferol daily. Urinary, biochemical, hemodynamic, and electrocardiographic parameters and renal function were assessed. Samples of the liver, heart, kidney, and arteries were collected to investigate redox status and perform histopathological analyses. All of the groups developed dyslipidemia and hepatic steatosis. Only the NEAD group developed arterial lesions that were compatible with fatty streaks. Renal function was significantly impaired in the LEAD and NOAD groups. These results indicate a viable alternative to induce atherogenesis and hepato-renal impairment in female rats. View Full-Text
Keywords: atherosclerosis; dyslipidemia; hepatic steatosis; kidney failure atherosclerosis; dyslipidemia; hepatic steatosis; kidney failure
Show Figures

Figure 1

MDPI and ACS Style

Guarnier, L.P.; Romão, P.V.M.; Palozi, R.A.C.; Silva, A.O.; Lorençone, B.R.; Marques, A.A.M.; dos Santos, A.C.; Souza, R.I.C.; Souza, K.D.; Lourenço, E.L.B.; Gasparotto Junior, A. Development of a Predictive Model to Induce Atherogenesis and Hepato-Renal Impairment in Female Rats. Biomolecules 2019, 9, 664.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop