Stanozolol promotes lipid deposition in the aorta through an imbalance in inflammatory cytokines and oxidative status in LDLr knockout mice fed a normal diet
Autor: | Silvia Cruz Goes Coutinho Haguihara, Raiana Maria Prucoli Falsoni, Cristiane Lyrio da Silva, Andrews Marques do Nascimento, Flávia de Souza Andrade Moraes, Tadeu Uggere de Andrade, Ewelyne Miranda de Lima, Dionisio Gonzaga Dubois Filho, Girlandia Alexandre Brasil |
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Rok vydání: | 2018 |
Předmět: |
Male
medicine.medical_specialty Normal diet medicine.medical_treatment Toxicology medicine.disease_cause Systemic inflammation 030226 pharmacology & pharmacy Proinflammatory cytokine Lipid peroxidation 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Anabolic Agents Internal medicine medicine Animals Stanozolol Aorta Pharmacology Inflammation Mice Knockout Cholesterol General Medicine Atherosclerosis Lipid Metabolism Lipoproteins LDL Disease Models Animal Oxidative Stress Endocrinology chemistry Receptors LDL Disease Progression Cytokines lipids (amino acids peptides and proteins) medicine.symptom Inflammation Mediators Oxidation-Reduction 030217 neurology & neurosurgery Anabolic steroid Oxidative stress medicine.drug |
Zdroj: | Basicclinical pharmacologytoxicology. 124(4) |
ISSN: | 1742-7843 |
Popis: | The aim of the study was to evaluate the effect of an anabolic steroid, stanozolol, in a model of atherosclerosis and to investigate the involvement of the modulation of the inflammatory cytokines and oxidative stress in vascular lipid deposition. Low-density lipid receptor-deficient (LDLr-/-) mice were fed a standard chow diet and were each week injected subcutaneously either saline (control C group) or 20 mg/kg stanozolol (S group). After 8 weeks, the levels of cholesterol, oxidized LDL (OxLDL) and cytokines were measured in plasma, lipid deposition in aorta was evaluated by en face analysis, and thiobarbituric acid-reactive substances and oxidation protein were determined in liver. The S group demonstrated increases in vascular lipid deposition, triglycerides and non-HDL cholesterol levels. Stanozolol increased tumour necrosis factor alpha (TNF-α) and decreased interleukin-10 as well as increased the TNF-α/IL-10 ratio. Furthermore, oxidative stress was observed in the S group, as indicated by an increase in the plasma OxLDL, as well as by lipid peroxidation and oxidation of proteins in the liver. Chronic treatment with stanozolol promoted lipid deposition in the LDLr-/- mice that could be attributed to a modification of the circulating cytokine levels and systemic oxidative stress. Our results suggest that the anabolic steroid stanozolol in the absence of functional LDL receptors by increasing systemic inflammation and oxidative stress may increase the risk of development and progression of atherosclerosis. |
Databáze: | OpenAIRE |
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