Influence of NF-κB inactivation with ammonium pyrrolidinedithiocarbamate on vasodilation of isolated aorta in rats with metabolic syndrome

Obesity has become an epidemic since almost 1/3 of the world’s population is overweight or obese. In many countries, overweight people account for 50–60% of the population. Obesity is considered as a risk factor for the development of metabolic syndrome and cardiovascular disease. The aim of the study was to investigate the contribution of NF-κB signaling to the endothelial dysfunction of the aorta in rats with metabolic syndrome. The metabolic syndrome model was reproduced by feeding rats with a high-calorie high-fat diet for 4 weeks. On day 14, one group of animals was injected with ammonium pyrrolidinedithiocarbamate (PDTC), a selective inhibitor of NF-κB. Rats were euthanized by decapitation under deep anesthesia and the thoracic aorta was isolated. In isolated aortic rings precontracted with phenylephrine, vasodilatory responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were measured. The results show that PDTC improved ACh-induced vasodilation and restored the activity of endothelial NO-synthase (eNOS) in rats with metabolic syndrome. The possible mechanism of action of PDTC involves inhibition of NF-κB–dependent inflammatory signaling, which contributes to improved endothelial function in metabolic disorders. These findings support the potential role of NF-κB signaling as a therapeutic target for vascular dysfunction in metabolic syndrome.