Diabetes Attenuates the Contribution of Endogenous Nitric Oxide but Not Nitroxyl to Endothelium Dependent Relaxation of Rat Carotid Arteries

Li, Jasmin Chendi; Velagic, Anida; Qin, Cheng Xue; Li, Mandy; Leo, Chen Huei; Kemp-Harper, Barbara K; Ritchie, Rebecca H.; Woodman, Owen L.

doi:10.3389/fphar.2020.585740

Cited by 11 publications

(6 citation statements)

References 113 publications

(165 reference statements)

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“…The level of non–endothelium‐dependent vasodilation was detected by using intraperitoneal injection of sodium nitroprusside (SNP; 0.05 mg/kg), and the level of endothelium‐dependent vasodilation was detected separately by using intraperitoneal injection of acetylcholine (Ach; 0.05 mg/kg) or INS (1 U/kg) [17–19]. Intraperitoneal injection of an equal amount of saline was performed as the vehicle Ctrl.…”

Section: Methodsmentioning

confidence: 99%

“…To our knowledge, our study is the first to uncover the harmful effect of ASP on the vascular endothelium and its involvement in lipid metabolism in obesity, which may point out a new direction for ASP as a therapeutic target for vascular diseases. 0.05 mg/kg), and the level of endothelium-dependent vasodilation was detected separately by using intraperitoneal injection of acetylcholine (Ach; 0.05 mg/kg) or INS (1 U/kg) [17][18][19]. Intraperitoneal injection of an equal amount of saline was performed as the vehicle Ctrl.…”

Section: What Does This Study Add?mentioning

confidence: 99%

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Asprosin aggravates vascular endothelial dysfunction via disturbing mitochondrial dynamics in obesity models

Yuan

Xiong

et al. 2023

Obesity

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Objective: The aim of the study was to investigate the contribution of asprosin (ASP), a fasting-induced hormone involved in metabolic disorders, to vascular endothelial dysfunction in obesity models.Methods: Primary rat thoracic aortic endothelial cells treated with palmitic acid and mice fed with a high-fat diet (HFD) were used as the obesity models. The role and mechanism of ASP in endothelial dysfunction were investigated by the means of morphologic, functional, and genetic analysis.Results: ASP aggravated the endothelial dysfunction induced by either palmitic acid in vitro or an HFD in vivo, characterized as the impairment of endotheliumdependent vasodilation, reduction of nitric oxide levels, elevation of malondialdehyde levels, and inhibition of phosphoinositide 3-kinase-AKT-endothelial nitric oxide synthase signaling. However, adipose conditional knockout of ASP or ASP neutralization significantly alleviated the endothelial dysfunction induced by an HFD. Mechanistically, ASP enhanced mitochondrial fission, and inhibition of the fission through knockdown of dynamin-related protein 1 (a fission-hallmark factor) rescued the endothelial dysfunction and the disturbance to mitochondrial dynamics induced by ASP. Conclusions:The findings demonstrate that ASP causes and even exacerbates vascular endothelial dysfunction through promoting mitochondrial fission in obesity, suggesting that ASP can act as an early predictive marker of blood vessel dysfunction and become a novel potential therapeutic target for obesity-related cardiovascular diseases.

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Section: Methodsmentioning

confidence: 99%

Section: What Does This Study Add?mentioning

confidence: 99%

Asprosin aggravates vascular endothelial dysfunction via disturbing mitochondrial dynamics in obesity models

Yuan

Xiong

et al. 2023

Obesity

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“…One of the biggest groups of naturally occurring polyphenolic substances, flavonoids, are well-recognised to possess several biological activities, including antioxidant, anti-inflammatory, and vasodilatory properties [ 7 , 8 , 9 ]. Given that oxidative stress and inflammation are common features reported in endothelial dysfunction, a critical and initiating factor for several vascular complications [ 10 , 11 , 12 , 13 ], flavonoids are widely considered as potential sources of natural product to exert beneficial effects on the cardiovascular system [ 14 ]. Indeed, several previous studies have shown that flavonoids present in orange peel waste (OPW) possessed antioxidant and anti-inflammatory properties [ 15 , 16 ] although less is known on the effects of OPW in endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

Green Extraction of Orange Peel Waste Reduces TNFα-Induced Vascular Inflammation and Endothelial Dysfunction

et al. 2022

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Orange peel waste (OPW) is known to contain an abundant amount of polyphenols compounds such as flavonoids, well-reported for their antioxidant and anti-inflammatory properties. While OPW is generally regarded as a food waste, the opportunity to extract bioactive compounds from these “wastes” arises due to their abundance, allowing the investigation of their potential effects on endothelial cells. Hence, this study aims to use a green extraction method and pressurized hot water extraction (PHWE) to extract bioactive compounds from OPW. Liquid chromatography with UV detection (LC/UV) and liquid chromatography mass spectrometry (LC/MS) were subsequently used to identify the bioactive compounds present. Through the optimization of the extraction temperature for PHWE, our results demonstrated that extraction temperatures of 60 °C and 80 °C yield distinct bioactive compounds and resulted in better antioxidant capacity compared to other extraction temperatures or organic solvent extraction. Despite having similar antioxidant capacity, their effects on endothelial cells were distinct. Specifically, treatment of endothelial cells with 60 °C OPW extracts inhibited TNFα-induced vascular inflammation and endothelial dysfunction in vitro, suggesting that OPW possess vasoprotective effects likely mediated by anti-inflammatory effects.

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“…In a diabetic rat model, injection of STZ increased ROS and caused endothelial cell dysfunction, which resulted in decreased formation of NO and cGMP in aortic tissue. Therefore, natural products that have antioxidant effects can be used to prevent endothelial cell damage in diabetes [ 17 , 18 , 19 ]. The antioxidants from natural products such as Cinnamomum cassia and Heterotrigona itama could be used as protection against endothelial cell dysfunction in diabetic complications, as they are shown to decrease ROS and increase the NOS, NO, and cGMP in rat aortic tissue that was given streptozotocin intraperitoneally [ 20 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanism of Fucoidan Nanoparticles as Protector on Endothelial Cell Dysfunction in Diabetic Rats’ Aortas

et al. 2023

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Antioxidants have an important role in protecting against diabetes complications such as vascular endothelial cell damage. Fucoidan has strong antioxidant properties, therefore the aim of this study was to investigate the protective mechanism of fucoidan nanoparticles through the pathway of antioxidant activity against streptozotocin-induced diabetic aortic endothelial cell dysfunction in rats. Fucoidan nanoparticles are made utilizing high-energy ball milling. This research consists of five groups, namely: control rats, rats were administered aquadest; diabetic rats, rats were administered streptozotocin (STZ); fucoidan nanoparticle rats, rats were administered STZ and fucoidan nanoparticles. Aortic tissue was collected for the evaluation of ROS (reactive oxygen species), Malondialdehyde (MDA), superoxide Dismutase (SOD), Glutathione Peroxidase (GPx), Nuclear factor erythroid-2-related factor 2 (Nrf2), Nitric Oxide (NO), cyclic Guanosine Monophosphate (cGMP), relaxation response of acetylcholine (Ach), and the diameter of the aorta. The size distribution of the fucoidan nanoparticles was 267.2 ± 42.8 nm. Administration of fucoidan nanoparticles decreased the levels of ROS and MDA, and increased the levels of SOD, levels of GPx, Nrf2 expression, NO levels, cGMP expression, the relaxation response of Ach, and lumen diameter of the aorta, which are significantly different when compared with diabetic rats, p < 0.05. In this study, we concluded that the mechanism pathway of fucoidan nanoparticles prevents aortic endothelial cell dysfunction in diabetic rats through antioxidant activity by reducing ROS and MDA and incrementing SOD levels, GPx levels, and Nrf2 expression. All of these can lead to an elevated relaxation response effect of Ach and an increase in the lumen diameter of the aorta, which indicates a protective effect of fucoidan nanoparticles on aortic endothelial cells.

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Diabetes Attenuates the Contribution of Endogenous Nitric Oxide but Not Nitroxyl to Endothelium Dependent Relaxation of Rat Carotid Arteries

Cited by 11 publications

References 113 publications

Asprosin aggravates vascular endothelial dysfunction via disturbing mitochondrial dynamics in obesity models

Asprosin aggravates vascular endothelial dysfunction via disturbing mitochondrial dynamics in obesity models

Green Extraction of Orange Peel Waste Reduces TNFα-Induced Vascular Inflammation and Endothelial Dysfunction

Molecular Mechanism of Fucoidan Nanoparticles as Protector on Endothelial Cell Dysfunction in Diabetic Rats’ Aortas

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