Universidade Estadual Paulista Júlio de Mesquita Filho Câmpus de Botucatu Faculdade de Medicina , Botucatu , SP - Brasil.
Universidade Federal de Mato Grosso , Sinop , MT - Brasil.
Arq Bras Cardiol. 2021 Jul;117(1):91-99. doi: 10.36660/abc.20190788.
Obesity is a chronic low-grade inflammation condition related to cardiac disorders. However, the mechanism responsible for obesity-related cardiac inflammation is unclear. The toll-like receptor 4 (TLR-4) belongs to a receptor of the transmembrane family responsible for the immune response whose activation stimulates the production of proinflammatory cytokines.
To test whether the activation of the TLR-4 receptor participates in the obesity cardiomyopathy process, due to cytokine production through NF-ĸB activation.
Male Wistar rats were randomized into two groups: the control group (C, n= 8 animals) that received standard diet/water and the obese group (OB, n= 8 animals) that were fed a high sugar-fat diet and water plus 25% of sucrose for 30 weeks. Nutritional analysis: body weight, adiposity index, food, water, and caloric intake. Obesity-related disorders analysis: plasma glucose, uric acid and triglycerides, HOMA-IR, systolic blood pressure, TNF-α in adipose tissue. Cardiac analysis included: TLR-4 and NF-ĸB protein expression, TNF-α and IL-6 levels. Comparison by unpaired Student's t-test or Mann- Whitney test with a p-value < 0.05 as statistically significant.
The OB group showed obesity, high glucose, triglycerides, uric acid, HOMA, systolic blood pressure, and TNF-α in adipose tissue. OB group presented cardiac remodeling and diastolic dysfunction. TLR-4 and NF-ĸB expression and cytokine levels were higher in OB.
Our findings conclude that, in an obesogenic condition, the inflammation derived from cardiac TLR-4 activation can be a mechanism able to lead to remodeling and cardiac dysfunction.
肥胖是一种与心脏疾病相关的慢性低度炎症状态。然而，导致肥胖相关心脏炎症的机制尚不清楚。 Toll 样受体 4（TLR-4）属于负责免疫反应的跨膜家族受体，其激活会刺激促炎细胞因子的产生。
检测 TLR-4 受体的激活是否通过 NF-ĸB 激活参与肥胖性心肌病过程，从而导致细胞因子的产生。
雄性 Wistar 大鼠随机分为两组：对照组（C 组，n=8 只动物）给予标准饮食/水，肥胖组（OB 组，n=8 只动物）给予高糖高脂肪饮食和水，外加 25%的蔗糖，持续 30 周。营养分析：体重、肥胖指数、食物、水和热量摄入。肥胖相关疾病分析：血浆葡萄糖、尿酸和甘油三酯、HOMA-IR、收缩压、脂肪组织中的 TNF-α。心脏分析包括：TLR-4 和 NF-ĸB 蛋白表达、TNF-α 和 IL-6 水平。采用配对学生 t 检验或曼-惠特尼检验进行比较，p 值<0.05 为统计学显著差异。
OB 组表现出肥胖、高血糖、甘油三酯、尿酸、HOMA、收缩压和脂肪组织中的 TNF-α。OB 组出现心脏重构和舒张功能障碍。OB 组 TLR-4 和 NF-ĸB 表达及细胞因子水平升高。
我们的研究结果表明，在肥胖条件下，心脏 TLR-4 激活引起的炎症可能是导致重构和心脏功能障碍的机制之一。
