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Melatonin reverses the loss of the anticontractile effect of perivascular adipose tissue in obese rats
Journal of Pineal Research ( IF 10.3 ) Pub Date : 2020-12-17 , DOI: 10.1111/jpi.12710
Natália A Gonzaga 1 , Wanessa M C Awata 1 , Sabrina P Ficher 1 , Victor O Assis 1 , Juliano V Alves 1 , Rita C Tostes 1 , Carlos R Tirapelli 1
Affiliation  

Perivascular adipose tissue (PVAT) undergoes functional changes in obesity. Increased oxidative stress is a central mechanism whereby obesity induces loss of the anticontractile effect of PVAT. Melatonin is an antioxidant that displays vasoprotective action in cardiovascular disease. Here, we sought to investigate whether melatonin would restore the anticontractile effect of periaortic PVAT in obesity. Male Wistar Hannover rats were treated for 10 weeks with a high‐calorie diet. Melatonin (5 mg/kg/d, p.o., gavage) was administered for 2 weeks. Functional findings showed that obesity‐induced loss of the anticontractile effect of PVAT and treatment with melatonin reversed this response. Tiron [a scavenger of superoxide anion (O2)] restored the anticontractile effect of PVAT in aortas from obese rats, suggesting a role for reactive oxygen species (ROS) in such response. Decreased superoxide dismutase (SOD) activity and augmented levels of ROS were detected in periaortic PVAT from obese rats. These responses were accompanied by decreased levels of nitric oxide (NO) in PVAT. Treatment with melatonin restored SOD activity, decreased ROS levels, and increased NO bioavailability in PVAT from obese rats. Here, we first reported the beneficial effects of melatonin in periaortic PVAT in obesity. Melatonin reversed the adverse effects of obesity in PVAT that included overproduction of ROS, reduced SOD activity, and decreased bioavailability of NO. Therefore, PVAT may constitute an important target for the treatment of obesity‐induced vascular dysfunction and melatonin emerges as a potential tool in the management of the vascular complications induced by obesity.

中文翻译:

褪黑激素逆转肥胖大鼠血管周围脂肪组织抗收缩作用的丧失

血管周围脂肪组织 (PVAT) 在肥胖时会发生功能变化。增加的氧化应激是肥胖导致 PVAT 抗收缩作用丧失的核心机制。褪黑激素是一种抗氧化剂,在心血管疾病中具有血管保护作用。在这里,我们试图调查褪黑激素是否会恢复主动脉周围 PVAT 对肥胖症的抗收缩作用。雄性 Wistar Hannover 大鼠接受高热量饮食治疗 10 周。褪黑激素(5 毫克/公斤/天,口服,管饲)给药 2 周。功能研究结果表明,肥胖引起的 PVAT 抗收缩作用的丧失和褪黑激素治疗逆转了这种反应。Tiron [超氧阴离子(O 2 -)] 恢复了 PVAT 在肥胖大鼠主动脉中的抗收缩作用,表明活性氧 (ROS) 在这种反应中的作用。在肥胖大鼠的主动脉周围 PVAT 中检测到超氧化物歧化酶 (SOD) 活性降低和 ROS 水平增加。这些反应伴随着 PVAT 中一氧化氮 (NO) 水平的降低。用褪黑激素处理可恢复肥胖大鼠 PVAT 中 SOD 活性、降低 ROS 水平并增加 NO 生物利用度。在这里,我们首先报告了褪黑激素对肥胖症主动脉周围 PVAT 的有益作用。褪黑激素逆转了 PVAT 肥胖的不利影响,包括 ROS 的过度产生、SOD 活性降低和 NO 生物利用度降低。所以,
更新日期:2021-02-15
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