Apocynin improves endothelial function and prevents the development of hypertension in fructose fed rat

Unger, Banappa S.; Patil, B. M.

doi:10.4103/0253-7613.58508

Cited by 26 publications

(5 citation statements)

References 23 publications

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“…Several studies indicate the possibly beneficial effect of some sweeteners for health [25, 26], but it is well known that fructose intake induces hypertension and impairs vascular contraction and relaxation [15, 27, 28]. In our study, high-fructose intake increased BP and body weight (Fig.…”

Section: Discussionsupporting

confidence: 51%

Acute Exposure to Fructose Impairs Endothelium-Dependent Relaxation via Oxidative Stress in Isolated Rat Aortic Rings

et al. 2020

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Introduction: Although both glucose and fructose are hexoses, their catabolism is quite different: the catabolism of fructose is initiated by ketohexokinase and is not regulated by negative feedback, which results in oxidative stress. Objective: We hypothesized that fructose impairs endothelium-dependent relaxation via oxidative stress in rat aortic rings. Methods: Sprague-Dawley rats were offered 20% fructose solution or tap water for 2 weeks, after which vascular reactivity was measured in isolated aortic rings. In a separate experiment, vascular reactivity was measured after acute exposure to ∼10 mM fructose in isolated aortic rings from untreated rats. Results: Although high-fructose intake statistically significantly increased blood pressure and body weight, it did not affect contraction and relaxation in aortic rings. The substitution of fructose for glucose in Krebs solution inhibited vascular relaxation in aortic rings, which was abolished by pretreatment with antioxidants. Decreasing the glucose concentration in Krebs solution inhibited vascular relaxation , whereas decreasing the fructose concentration in Krebs solution improved vascular relaxation in the aortic rings. Pretreatment with antioxidants improved the vascular relaxation in Krebs solution with fructose substituted for glucose. Conclusions: These results indicate that fructose impairs endothelium-dependent relaxation via oxidative stress in isolated rat aortic rings.

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Section: Discussionsupporting

confidence: 51%

Acute Exposure to Fructose Impairs Endothelium-Dependent Relaxation via Oxidative Stress in Isolated Rat Aortic Rings

et al. 2020

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“…To prevent synthesis and influence of prostaglandins, the experiment was conducted in the presence of 10 mM indomethacin (Unger and Patil 2009). …”

Section: Vascular Reactivity Measurementsmentioning

confidence: 99%

Effects of fisetin on hyperhomocysteinemia-induced experimental endothelial dysfunction and vascular dementia

Kumar

Ravula

Kumar

et al. 2017

Can. J. Physiol. Pharmacol.

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This study was designed to investigate the effects of fisetin (FST) on hyperhomocysteinemia (HHcy)-induced experimental endothelial dysfunction (ED) and vascular dementia (VaD) in rats. Wistar rats were randomly divided into 8 groups: control, vehicle control, l-methionine, FST (5, 10, and 25 mg/kg, p.o.), FST-per se (25 mg/kg, p.o.), and donepezil (0.1 mg/kg, p.o.). l-Methionine administration (1.7 g/kg, p.o.) for 32 days induced HHcy. ED and VaD induced by HHcy were determined by vascular reactivity measurements, behavioral analysis using Morris water maze and Y-maze, along with a biochemical and histological evaluation of thoracic aorta and brain tissues. Administration of l-methionine developed behavioral deficits; triggered brain lipid peroxidation (LPO); compromised brain acetylcholinesterase activity (AChE); and reduced the levels of brain superoxide dismutase (SOD), brain catalase (CAT), brain reduced glutathione (GSH), and serum nitrite; and increased serum homocysteine and cholesterol levels. These effects were accompanied by decreased vascular NO bioavailability, marked intimal thickening of the aorta, and multiple necrotic foci in brain cortex. HHcy-induced alterations in the activities of SOD, CAT, GSH, AChE, LPO, behavioral deficits, ED, and histological aberrations were significantly attenuated by treatment with fisetin in a dose-dependent manner. Collectively, our results indicate that fisetin exerts endothelial and neuroprotective effects against HHcy-induced ED and VaD.

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“…In streptozotocin- (STZ-) induced murine models and db/db mice, which represent T1D and T2D respectively, it has been shown that the expression and activity of these Nox isoforms and their regulatory subunits are greatly upregulated in the aortic region and mesenteric vascular bed [ 22 , 27 – 29 ]. Furthermore, this upregulation was associated with increased oxidative stress and attenuated eNOS expression and eNOS-derived EDNO [ 29 , 30 ]. More recently, it was shown that the increased expression of the Nox catalytic subunits, in particular Nox2, is directly related to eNOS uncoupling and eNOS-derived superoxide production in carotid arteries of diabetic rats [ 31 ].…”

Section: Diabetes-mediated Endothelial Dysfunctionmentioning

confidence: 99%

“…Several novel small-molecule and peptide inhibitors of the NOX enzymes have been developed and shown to have promise in experimental studies [ 75 ]. Indeed, treatment with the Nox inhibitor, apocynin, reversed the upregulation of Nox isoforms, increased eNOS function, and reduced endothelial dysfunction in STZ-induced and fructose-fed rats [ 29 , 30 ]. Apocynin was also effective in improving vascular function induced by hyperglycaemia in a non-obese model of T2D [ 76 ].…”

Section: Targeting Oxidant and Antioxidant Pathways In Diabetesmentioning

confidence: 99%

Targeting Endothelial Dysfunction in Vascular Complications Associated with Diabetes

Sharma

Bernatchez

2012

International Journal of Vascular Medicine

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Cardiovascular complications associated with diabetes remain a significant health issue in westernized societies. Overwhelming evidence from clinical and laboratory investigations have demonstrated that these cardiovascular complications are initiated by a dysfunctional vascular endothelium. Indeed, endothelial dysfunction is one of the key events that occur during diabetes, leading to the acceleration of cardiovascular mortality and morbidity. In a diabetic milieu, endothelial dysfunction occurs as a result of attenuated production of endothelial derived nitric oxide (EDNO) and augmented levels of reactive oxygen species (ROS). Thus, in this review, we discuss novel therapeutic targets that either upregulate EDNO production or increase antioxidant enzyme capacity in an effort to limit oxidative stress and restore endothelial function. In particular, endogenous signaling molecules that positively modulate EDNO synthesis and mimetics of endogenous antioxidant enzymes will be highlighted. Consequently, manipulation of these unique targets, either alone or in combination, may represent a novel strategy to confer vascular protection, with the ultimate goal of improved outcomes for diabetes-associated vascular complications.

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Apocynin improves endothelial function and prevents the development of hypertension in fructose fed rat

Cited by 26 publications

References 23 publications

Acute Exposure to Fructose Impairs Endothelium-Dependent Relaxation via Oxidative Stress in Isolated Rat Aortic Rings

Acute Exposure to Fructose Impairs Endothelium-Dependent Relaxation via Oxidative Stress in Isolated Rat Aortic Rings

Effects of fisetin on hyperhomocysteinemia-induced experimental endothelial dysfunction and vascular dementia

Targeting Endothelial Dysfunction in Vascular Complications Associated with Diabetes

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