Manzoni A G, Passos D F, Doleski P H, Leitemperger J W, Loro V L, Leal D B R
Laboratório de Imunobiologia Experimental e Aplicada (LABIBIO), Departamento de Microbiologia e Parasitologia, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
Programa de Pós-Graduação em Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
Cardiovasc Drugs Ther. 2020 Dec;34(6):813-821. doi: 10.1007/s10557-020-07034-5. Epub 2020 Jul 11.
Hyperlipidemia, characterized by an increase in circulating lipid levels, doubles the chance of developing cardiovascular diseases. It prompts inflammation, immune activation, and oxidative stress in the bloodstream and organs of rats. Thus, we theorized that the metabolism of purines, an immunomodulatory mechanism, is altered in cells involved in the development of cardiovascular diseases.
Therefore, we induced acute hyperlipidemia in Wistar rats with Poloxamer-407 and euthanized the animals 36 h later. The leucocyte differential, the rate of purine metabolism on the surface of platelets and heart cells, and markers of oxidative stress in the heart tissue were evaluated. These parameters were also assessed in animals pretreated for 30 days with curcumin and/or rutin.
Hyperlipidemia increased the hydrolyses of adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) in platelets. In heart cells, the metabolism of ATP and adenosine (ADO) were increased, while ADP hydrolysis was reduced. Additionally, lipid damage and antioxidant defenses were increased in heart homogenates. Hyperlipidemic rats also exhibited a reduced percentage of eosinophils and lymphocytes.
Together, these findings are indicative of an increased risk of developing cardiovascular diseases in hyperlipidemic rats. The pretreatments with antioxidants reverted some of the changes prompted by hyperlipidemia preventing detrimental changes in the cells and tissues. Graphical Abstract.
高脂血症以循环脂质水平升高为特征,会使患心血管疾病的几率增加一倍。它会引发大鼠血液和器官中的炎症、免疫激活和氧化应激。因此,我们推测,嘌呤代谢作为一种免疫调节机制,在参与心血管疾病发展的细胞中会发生改变。
因此,我们用泊洛沙姆 - 407诱导Wistar大鼠急性高脂血症,并在36小时后对动物实施安乐死。评估白细胞分类、血小板和心脏细胞表面的嘌呤代谢率以及心脏组织中的氧化应激标志物。还对用姜黄素和/或芦丁预处理30天的动物进行了这些参数的评估。
高脂血症增加了血小板中三磷酸腺苷(ATP)、二磷酸腺苷(ADP)和一磷酸腺苷(AMP)的水解。在心脏细胞中,ATP和腺苷(ADO)的代谢增加,而ADP水解减少。此外,心脏匀浆中的脂质损伤和抗氧化防御增加。高脂血症大鼠的嗜酸性粒细胞和淋巴细胞百分比也降低。
总之,这些发现表明高脂血症大鼠患心血管疾病的风险增加。抗氧化剂预处理逆转了高脂血症引发的一些变化,防止细胞和组织发生有害变化。图形摘要。