Treatment with sodium nitroprusside improves the endothelial function in aortic rings with endothelial dysfunction

Buzinari, Tereza Cristina; Oishi, Jorge; Moraes, Thiago Francisco de; Vatanabe, Izabela Pereira; Selistre-de-Araújo, Heloísa Sobreiro; Pestana, Cezar Rangel; Rodrigues, Gerson Jhonatan

doi:10.1016/j.ejps.2017.04.022

Cited by 13 publications

(8 citation statements)

References 33 publications

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“…CP (5 mg/mL; CAS 15663-27-1) was purchased from Jiangsu Hansoh Pharmaceutical Co. Ltd., China, 16 and RUT (purity >98%; CAS 153-18-4) was purchased from Jingzhu Technology Co. Ltd., China. Methyl thiazolyl tetrazolium (MTT; CAS 298-93-1) was purchased from Sigma-Aldrich (Massachusetts, USA), 17 and Hoechst33258 kit, dichlorodihydrofluorescein diacetate (DCFH-DA),NAC, and cleaved-caspase-3 antibody were purchased from the Beyotime Institute of Biotechnology (Nanjing, China). Malonic dialdehyde (MDA) and superoxide dismutase (SOD) kits were purchased from Jiancheng Biological Institute (Nanjing, China).…”

Section: Methodsmentioning

confidence: 99%

Effect of rutin on cisplatin-induced damage in human mesangial cells via apoptotic pathway

Zhang

Wang

et al. 2018

Hum Exp Toxicol

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Cisplatin (CP) is one of the most effective and widely used compounds in the treatment of disease, including cancer, but is known to induce toxicity in patients. Rutin (RUT) is a flavonoid glycoside from Sophora japonica L. that has been shown to possess antioxidative, anti-inflammatory, and antiviral properties. RUT is also known to attenuate cardiotoxicity, isoproterenol-induced cardiac fibrosis, and ischemia/reperfusion-associated hemodynamic alteration, and prevents high glucose-induced renal glomerular endothelial hyperpermeability. In this study, we investigated the effect of RUT on CP-induced nephrotoxicity. CP was used to induce toxicity in human mesangial cells (HMCs), HMCs were pretreated with different concentrations of RUT before being exposed to 10 μg/mL of CP. A positive group was pretreated with antioxidant agent N-acetylcysteine prior to CP administration. At doses between 12.5 and 25 μM, RUT prevented CP-induced reduction in cell viability. Treatment with RUT suppressed intracellular reactive oxygen species and malonic dialdehyde levels and inhibited cell apoptosis. RUT reversed the CP-induced upregulation of p53, cleaved-caspase-3, and increased pro-caspase-3 and pro-caspase-9 levels. In conclusion, the RUT can relieve CP-induced nephrotoxicity by inhibiting the p53/caspase signaling pathway.

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Section: Methodsmentioning

confidence: 99%

Effect of rutin on cisplatin-induced damage in human mesangial cells via apoptotic pathway

Zhang

Wang

et al. 2018

Hum Exp Toxicol

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“…Images from 10 different fields were captured in which the DHE labeling (fluorescent probe for reactive oxygen species) was analyzed, thus generating three images: ROS labeling, cells in DIC, and image merging. This protocol was similar to that previously described (17).…”

Section: Effect Of Pv3 On Human Endothelial Cellsmentioning

confidence: 99%

Oxidonitrergic and antioxidant effects of a low molecular weight peptide fraction from hardened bean (Phaseolus vulgaris) on endothelium

Graziani

Ribeiro

Cruz

et al. 2021

Braz J Med Biol Res

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About 3000 tons of beans are not used in human food due to hardening. Several studies on bean-derived bioactive peptides have shown potential to treat some diseases, including those relying on oxidative dysfunctions. We assessed the effects of peptides extracted from hardened bean Phaseolus vulgaris (PV) on reactive oxygen species (ROS) and nitric oxide (NO) production, cytotoxic and cytoprotective effects in endothelial cells, and oxidonitrergic-dependent vasodilating effects. Extract was composed by peptide fraction <3 kDa (PV3) from hardened common bean residue. PV3 sequences were obtained and analyzed with bioinformatics. Human umbilical vein endothelial cells were treated with 10, 20, 30, and 250 µg/mL PV3. Oxidative stress was provoked by 3% H 2 O 2 . Cytotoxicity and cytoprotective effects were evaluated by MTT assay, whereas, ROS and NO were quantified using DHE and DAF-FM fluorescent probes by confocal microscopy. NO- and endothelium-dependent vasodilating effects of PV3 were assessed in isolated aortic rings. We found 35 peptides with an average mass of 1.14 kDa. There were no cell deaths with 10 and 20 μg/mL PV3. PV3 at 30 μg/mL increased cell viability, while cytotoxicity was observed only with 250 μg/mL PV3. PV3 at 10 μg/mL was able to protect cells from oxidative stress. PV3 also increased NO release without causing cell death. It also reduced relative ROS production induced by H 2 O 2 . PV3 vasodilating effects relied on endothelium-dependent NO release. PV3 obtained from low-commercial-value bean displays little cytotoxicity and exerts antioxidant effects, whereas it increases endothelial NO release.

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“…Sodium Nitroprusside (SNP) is a powerful vasodilator subordinate to the nitro vasodilator and can directly relax the vascular smooth muscle of the small arteries and veins [ 19 ]. SNP is the direct donor of NO, which has the powerful function of relaxing the vascular smooth muscle as well as anti-inflammatory and anti-platelet aggregation [ 20 ]. ACH (acetylcholine) promotes the release of NO from vascular endothelial cells, which leads to the relaxation of adjacent smooth muscle cells [ 21 ].…”

Section: Resultsmentioning

confidence: 99%

Leonurine Attenuates Obesity-Related Vascular Dysfunction and Inflammation

Shi

Zhang

et al. 2022

Antioxidants

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Oxidative stress in adipose tissue is a crucial pathogenic mechanism of obesity-associated cardiovascular diseases. Chronic low-grade inflammation caused by obesity increases ROS production and dysregulation of adipocytokines. Leonurine (LEO) is an active alkaloid extracted from Herba Leonuri and plays a protective role in the cardiovascular system. The present study tested whether LEO alleviates inflammation and oxidative stress, and improves vascular function in an obese mouse model. Here, we found that obesity leads to inflammation and oxidative stress in epididymal white adipose tissue (EWAT), as well as vascular dysfunction. LEO significantly improved inflammation and oxidative stress both in vivo and in vitro. Obesity-induced vascular dysfunction was also improved by LEO as evidenced by the ameliorated vascular tone and decreased mesenteric artery fibrosis. Using mass spectrometry, we identified YTHDF1 as the direct target of LEO. Taken together, we demonstrated that LEO improves oxidative stress and vascular remodeling induced by obesity and targets YTHDF1, raising the possibility of LEO treating other obesity-related metabolic syndromes.

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Treatment with sodium nitroprusside improves the endothelial function in aortic rings with endothelial dysfunction

Cited by 13 publications

References 33 publications

Effect of rutin on cisplatin-induced damage in human mesangial cells via apoptotic pathway

Effect of rutin on cisplatin-induced damage in human mesangial cells via apoptotic pathway

Oxidonitrergic and antioxidant effects of a low molecular weight peptide fraction from hardened bean (Phaseolus vulgaris) on endothelium

Leonurine Attenuates Obesity-Related Vascular Dysfunction and Inflammation

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