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

机译:诱导雌性大鼠动脉粥样硬化和肝肾损害的预测模型的建立。

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摘要

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- -arginine methyl ester hydrochloride ( -NAME; LEAD), and ovariectomized rats that received an atherogenic diet and oral -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.
机译:近几十年来,用于治疗血脂异常和动脉粥样硬化的治疗方法已经发生了根本性的变化。无可否认,这一进步的一部分源于基础生物医学研究,该研究提供了对新治疗靶标的更好理解和鉴定。这项工作的目的是建立在雌性Wistar大鼠中诱发动脉粥样硬化和肝肾损害的模型。以下各组分别接受60天的治疗:对照动物,接受动脉粥样硬化饮食(NEAD)的非切除卵巢的大鼠,接受动脉粥样硬化饮食(NOAD)的切除卵巢的大鼠,接受动脉粥样硬化饮食的非切除卵巢的大鼠和口服Nω -硝基-精氨酸甲酯盐酸盐(-NAME; LEAD),以及接受了动脉粥样化饮食和口服-NAME(LOAD)的去卵巢大鼠。 NEAD,NOAD,LEAD和LOAD组的动物每天也接受甲巯咪唑和胆钙化固醇。评估尿,生化,血液动力学和心电图参数以及肾功能。收集肝脏,心脏,肾脏和动脉的样本以调查氧化还原状态并进行组织病理学分析。所有组均发生血脂异常和肝脂肪变性。只有NEAD组出现了与脂肪条纹相容的动脉病变。 LEAD和NOAD组的肾功能明显受损。这些结果表明在雌性大鼠中诱导动脉粥样硬化和肝肾损害的可行选择。

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