Abstract
Vascular complications are the leading cause of morbidity and mortality in patients with diabetes. Quercetin is an important flavonoid with antioxidant and anti-inflammatory activity. Here, the effect of quercetin on diabetes-induced exaggerated vasoconstriction in insulin deficient and insulin resistant rat models was investigated. Insulin deficiency was induced by streptozotocin while, insulin resistance by fructose. Rats were left 8 weeks or 12 weeks after STZ or fructose administration respectively. Quercetin was daily administered in the last 6 weeks. Then, tail blood pressure (BP) was recorded in conscious animals; concentration-response curves for phenylephrine (PE) and KCl were studied in thoracic aorta rings. Non-fasting blood glucose level, serum insulin level, insulin resistance index, serum tumour necrosis factor-α (TNF-α) and serum C-reactive protein (CRP) were determined. Nuclear transcription factor-κB (NF-κB) was assessed by immunofluorescence technique. Histopathological examination was also performed. The results showed that quercetin protected against diabetes-induced exaggerated vasoconstriction and reduced the elevated blood pressure. In addition, quercetin inhibited diabetes associated adventitial leukocyte infiltration, endothelial pyknosis and increased collagen deposition. These effects were accompanied with reduction in serum level of both TNF-α and CRP and inhibition of aortic NF-κB by quercetin in both models of diabetes. On the other hand, quercetin did not affect glucose level in any of the used diabetic models. This suggests that the protective effect of quercetin is mediated by its anti-inflammatory effect rather than its metabolic effects. In summary, quercetin is potential candidate to prevent diabetic vascular complications in both insulin deficiency and resistance via its inhibitory effect on inflammatory pathways especially NF-κB signaling.
Highlights
In the last decade the incidence and prevalence of diabetes has risen steeply
We have previously reported an important role of Tumour necrosis factor-a (TNF-a) in the pathogenesis of vascular disease in insulin resistance [8]
(50 mg/kg/day) in the last 6 weeks to normal animals did not affect either body weight, blood glucose, insulin level, HOMA-IR or circulating TNF-a and C-reactive protein (CRP) levels compared with control group
Summary
In the last decade the incidence and prevalence of diabetes has risen steeply. the large number of diabetic patients and the increased mortality and morbidity rates due to increased cardiovascular diabetic complications have got a great attention [1]. While the main goal is prevention of diabetes development and curing the disease, prevention and treatment of complications are important [1]. Studies in both animal and human diabetics have shown alteration of several factors that may be fundamental in mediating structural and functional deficits at both the early and the late stages of the disease [2]. There is increasing evidence indicating that there is a strong relationship between inflammatory processes and the development and progression of diabetic complications [3]. In vitro studies have shown that CRP has a direct proinflammatory effect on human endothelial cells and affects endothelial function [13]
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