Protective effect of resveratrol and quercetin on in vitro-induced diabetic mouse corpus cavernosum

Boydens, Charlotte; Pauwels, Bart; Daele, Laura Vanden; Voorde, Johan Van de

doi:10.1186/s12933-016-0366-9

Cited by 26 publications

(16 citation statements)

References 47 publications

(78 reference statements)

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“…Furthermore, pretreatment of MAECs with the inhibitor of class I and II histone deacetylase (HDAC), trichostatin A, was able to abolish the MGO effect on miR-190a expression, suggesting HDAC involvement. Consistent with previous findings proving the role of MGO in insulin-sensitivity and vascular function [ 53 , 55 , 78 ], the rescue of miR-190a levels we observed in MAECs upon the co-treatment with MGO and AG, revealed that MGO-modified proteins are critical in determining MGO-induced down-regulation of miR-190a.…”

Section: Mgo-induced Insulin-resistance: a Link To Endothelial Dyssupporting

confidence: 92%

“…This effect is attenuated by the MGO scavengers aminoguanidine (AG) and N -acetyl-cisteine (NAC) [ 52 ], via the inhibition of NADPH oxidase [ 53 ], and is prevented by Glo1 over-expression [ 54 ]. A protective effect of anti-oxidants such as polyphenols has been reported to prevent MGO-dependent impairment of NO release, improving endothelium-mediated relaxation in mouse corpora cavernosa [ 55 ]. A proposed mechanism by which MGO increases reactive oxygen species (ROS), promoting the apoptotic process, involves the reduced transcription of the cytoprotective protein thioredoxin [ 56 ].…”

Section: Effect Of Mgo Accumulation On Vascular Functionmentioning

confidence: 99%

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Methylglyoxal-Glyoxalase 1 Balance: The Root of Vascular Damage

Nigro

Leone

Raciti

et al. 2017

IJMS

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The highly reactive dicarbonyl methylglyoxal (MGO) is mainly formed as byproduct of glycolysis. Therefore, high blood glucose levels determine increased MGO accumulation. Nonetheless, MGO levels are also increased as consequence of the ineffective action of its main detoxification pathway, the glyoxalase system, of which glyoxalase 1 (Glo1) is the rate-limiting enzyme. Indeed, a physiological decrease of Glo1 transcription and activity occurs not only in chronic hyperglycaemia but also with ageing, during which MGO accumulation occurs. MGO and its advanced glycated end products (AGEs) are associated with age-related diseases including diabetes, vascular dysfunction and neurodegeneration. Endothelial dysfunction is the first step in the initiation, progression and clinical outcome of vascular complications, such as retinopathy, nephropathy, impaired wound healing and macroangiopathy. Because of these considerations, studies have been centered on understanding the molecular basis of endothelial dysfunction in diabetes, unveiling a central role of MGO-Glo1 imbalance in the onset of vascular complications. This review focuses on the current understanding of MGO accumulation and Glo1 activity in diabetes, and their contribution on the impairment of endothelial function leading to diabetes-associated vascular damage.

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Section: Mgo-induced Insulin-resistance: a Link To Endothelial Dyssupporting

confidence: 92%

Section: Effect Of Mgo Accumulation On Vascular Functionmentioning

confidence: 99%

Methylglyoxal-Glyoxalase 1 Balance: The Root of Vascular Damage

Nigro

Leone

Raciti

et al. 2017

IJMS

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“…EDHF requires triggering by the hyperpolarization of endothelium to be activated. Some papers have reported on the significance of EDHF to endothelium-dependent relaxation which is compromised due to endothelial dysfunction in streptozotocin (STZ)-induced rats [17, 21, 22]. As we have known, KCa3.1 mediates the hyperpolarization of endothelium, and is considered to be critical in initializing EDHF–dilator responses in endothelium-dependent relaxation [18, 23, 24].…”

Section: Introductionmentioning

confidence: 99%

Crocin Improves the Endothelial Function Regulated by Kca3.1 Through ERK and Akt Signaling Pathways

Yang

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Based on the protective effect of crocin against cardiovascular diseases, we hypothesize that crocin could improve endothelial function through activating the eNOS(endothelial nitric oxide synthase) /NO pathway and/or the intermediate-conductance Ca²⁺-activated K⁺ channels (KCa3.1). Methods: In this study, rat aortic rings were used to assess the regulatory effect of crocin on vascular tone and nitric oxide, prostacyclin, and KCa3.1, all endothelial vasodilators, were analyzed for effects by crocin. The expression profiles of p-eNOS, total-eNOS, p-ERK, total-ERK, p-Akt, total-Akt, KCa3.1, CD31, thrombomodulin, ICAM-1 and VCAM-1 were tested by western blotting. KCa3.1 was also analyzed by qPCR and immunofluorescence staining. Fluorescence and confocal microscopy were used to determine NO generation and intracellular Ca²⁺. Both EdU and MTT assays were used to evaluate cell viability. Cellular migration was assessed using transwell assay. Results: Crocin relaxed pre-contracted artery rings through either NO or KCa3.1, but not PGI, in an endothelium-dependent manner. Furthermore, crocin increased p-eNOS, total-eNOS expression and NO production as well as intracellular Ca²⁺ in both HUVECs and HUAECs (Human Umbilical Artery Endothelial cells). Crocin also stimulated the expression of CD31, thrombomodulin and vascular cell adhesion molecule 1 (VCAM-1), as well as increased cellular proliferation and migration in vitro. Interestingly, we determined for the first time that by blocking or silencing KCa3.1 there was inhibition of crocin induced upregulation of p-eNOS and total-eNOS. Correspondingly, the KCa3.1 inhibitor TRAM-34 also reduced the expression of CD31, thrombomodulin and VCAM-1, as well as diminished intracellular Ca²⁺, cellular proliferation and migration. Finally, crocin stimulated the expression of p-ERK, total-ERK, p-Akt and total-Akt, however suppression of MEK and Akt inhibited this expression profile in endothelial cells. Conclusion: In the present study, these data strongly support the hypothesis that crocin could improve endothelial function through stimulation of the eNOS/NO pathway and other endothelial markers. This functional improvement is regulated by KCa3.1 via the MEK/ERK and PI3K/Akt signaling pathway.

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“…The clinical trial was conducted with 42 healthy young male Japanese volunteers in Kumamoto, Japan. The following inclusion criteria were used for recruitment: (1) men over 20 years of age, (2) having no history of smoking and (3) having no history of diseases that alter the metabolism and/or excretion of drugs (such as gastroenterological, cardiovascular, pulmonary or hepatic diseases). In addition, the following exclusion criteria were applied: (1) a history of allergy to any foods and drugs, (2) eating functional foods routinely involved in the metabolism of glucose and/or lipids, (3) drinking red wine routinely, (4) having taken part in another clinical trial within three months and (5) taking any internal medication within one week before the start of the clinical trial through the end of the clinical trial.…”

Section: Participants and Clinical Trial Designmentioning

confidence: 99%

Melinjo seed extract increases adiponectin multimerization in physiological and pathological conditions

Oniki

Kawakami

Nakashima

et al. 2020

Sci Rep

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Melinjo seed extract (MSe) contains large amounts of polyphenols, including dimers of trans-resveratrol (e.g. gnetin c, L, gnemonoside A, B and D), and has been shown to potentially improve obesity. However, there is no clinical evidence regarding the anti-obesity effects of MSE, and its mechanisms are also unclear. We investigated the hypothesis that MSe supplementation increases the adiponectin (Apn) multimerization via the up-regulation of disulfide bond A oxidoreductase-like protein (DsbA-L) under either or both physiological and obese conditions. To investigate the effect of MSE on the physiological condition, 42 healthy young volunteers were enrolled in a randomized, double-blind placebo-controlled clinical trial for 14 days. The participants were randomly assigned to the MSE 150 mg/day, MSE 300 mg/day or placebo groups. Furthermore, in order to investigate the effect of MSE on APN levels under obese conditions, we administered MSE powder (500 or 1000 mg/kg/day) to control-diet-or high-fat-diet (HFD)-fed C57BL/6 mice for 4 weeks. All participants completed the clinical trial. The administration of MSE 300 mg/day was associated with an increase in the ratio of HMW/ total Apn in relation to the genes regulating Apn multimerization, including DsbA-L. furthermore, this effect of MSE was more pronounced in carriers of the DsbA-L rs191776 G/T or T/T genotype than in others. in addition, the administration of MSe to HfD mice suppressed their metabolic abnormalities (i.e. weight gain, increased blood glucose level and fat mass accumulation) and increased the levels of total and HMW Apn in serum and the mRnA levels of ADIPOQ and DsbA-L in adipose tissue. the present study suggests that MSE may exert beneficial effects via Apn multimerization in relation to the induction of DsbA-L under both physiological and obese conditions. Melinjo (Gnetum gnemon L.) is a gymnosperm native of Indonesia, and its seeds have long been eaten by the people of Indonesia 1. Melinjo seed extract (MSE) contains large amounts of polyphenols, including trans-resveratrol, gnetin C (dimer of trans-resveratrol), gnemonoside A (di-glucoside from gnetin C) and gnemonoside D (mono-glucoside from gnetin C), gnemonoside C (mono-glycoside from gnetin C) and gnetin L (derivative of gnetin C) 1. Resveratrols, in particular trans-resveratrol, have been reported to have diverse health benefits, demonstrating utility for treating aging-related diseases, including cancer, cardiovascular disease, type 2 diabetes and neurodegenerative disease in animal studies 2-4 ; however, its health benefits in humans are still controversial. One reason for this lack of certainty regarding its effects may be the rapid and presystemic metabolism of

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Protective effect of resveratrol and quercetin on in vitro-induced diabetic mouse corpus cavernosum

Cited by 26 publications

References 47 publications

Methylglyoxal-Glyoxalase 1 Balance: The Root of Vascular Damage

Methylglyoxal-Glyoxalase 1 Balance: The Root of Vascular Damage

Crocin Improves the Endothelial Function Regulated by Kca3.1 Through ERK and Akt Signaling Pathways

Melinjo seed extract increases adiponectin multimerization in physiological and pathological conditions

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