RESUMEN
Hyperlipidemia is one of the major risk factors for atherosclerosis and ischemic heart disease. Chromium (Cr) mineral is playing a crucial role in glucose and lipid homeostasis. The aim of this study was to evaluate the protective effects of combined chromium picolinate (CrPic) and atorvastatin treatment against hyperlipidemia-induced cardiac injury. Seventy-five male albino rats were divided into five groups (15 rats each). Hyperlipidemia was induced by intraperitoneal injection of a single dose of Triton X-100 (300 mg/kg body weight (b.w) (group ÐÐ). Treatment of hyperlipidemic rats was induced by daily administration of CrPic at a dose of 200 µg/kg b.w/day (group ÐÐÐ), atorvastatin at a dose of 10â mg/kg/day (group IV), and combined treatment with both (group V) by gavage for 7 days. At the end of experiment, serum and heart tissues were obtained. Hyperlipidemia was confirmed by histopathology of heart tissues, marked serum dyslipidemia, increased atherogenic indices, and values of ischemia-modified albumin. In addition to increased values of proprotein convertase subtilisin/kexin type 9, activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase enzyme and high relative expression levels of pentraxin-3 were observed. However, paraoxonase-1 activity was markedly decreased in the hyperlipidemic group. Significant improvement in all assessed parameters was observed in the rat group treated with both CrPic and atorvastatin. It can be concluded that combined CrPic and atorvastatin treatments had synergistic cardioprotective effects against hyperlipidemia which may be through modulating atherosclerosis as well as cardiac and aortic damage and/or activation of anti-inflammatory and anti-oxidant pathways, thus reversing endothelial dysfunction.
Asunto(s)
Atorvastatina/agonistas , Cromo/uso terapéutico , Suplementos Dietéticos , Modelos Animales de Enfermedad , Interacciones Alimento-Droga , Hiperlipidemias/dietoterapia , Hipolipemiantes/uso terapéutico , Animales , Aorta/efectos de los fármacos , Aorta/metabolismo , Aorta/patología , Atorvastatina/uso terapéutico , Biomarcadores/sangre , Biomarcadores/metabolismo , Proteína C-Reactiva/agonistas , Proteína C-Reactiva/genética , Proteína C-Reactiva/metabolismo , Cardiotónicos/agonistas , Cardiotónicos/uso terapéutico , Cromo/agonistas , Terapia Combinada , Regulación de la Expresión Génica/efectos de los fármacos , Ventrículos Cardíacos/efectos de los fármacos , Ventrículos Cardíacos/metabolismo , Ventrículos Cardíacos/patología , Hiperlipidemias/tratamiento farmacológico , Hiperlipidemias/metabolismo , Hiperlipidemias/patología , Hipolipemiantes/química , Lipoproteínas LDL/sangre , Masculino , Octoxinol , Ácidos Picolínicos/administración & dosificación , Distribución Aleatoria , Ratas Sprague-Dawley , Albúmina Sérica Humana , Componente Amiloide P Sérico/agonistas , Componente Amiloide P Sérico/genética , Componente Amiloide P Sérico/metabolismoRESUMEN
Enterococcus faecium is an emerging pathogen that causes infections in hospitalized patients with various co-morbid diseases. These underlying diseases are often associated with an acute-phase response that renders patients vulnerable to nosocomial infections. To study the influence of the acute-phase response induced by sterile tissue injury on host defence against E. faecium, mice were injected subcutaneously with either turpentine or casein 1 day before intraperitoneal infection with E. faecium. Control mice were subcutaneously injected with saline or sodium bicarbonate, respectively. Turpentine and casein induced an acute-phase response as reflected by increases in the plasma concentrations of interleukin-6, serum amyloid P and C3. A pre-existent acute-phase response in mice was associated with a strongly reduced capacity to clear E. faecium, resulting in prolonged bacteraemia for several days. The inflammatory response to E. faecium was impaired in mice with an acute-phase response, as shown by reduced capacity to mount a neutrophilic leucocytosis in peripheral blood and by decreased local cytokine concentrations. These data indicate that the acute-phase response impairs host defence against E. faecium, suggesting that this condition may contribute to the increased vulnerability of critically ill patients to enterococcal infections.