Oxidatív stressz és atherosclerosis

Stark, J. M.

doi:10.1556/650.2015.30201

Cited by 17 publications

(14 citation statements)

References 11 publications

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“…Endothelial dysfunction plays a key role in cardiovascular diseases. The imbalance between the production of ROS and their effective removal by non-enzymatic and enzymatic antioxidant systems could induce endothelial dysfunction through inducing injury, apoptosis and necrosis of endothelial cells, promoting accumulation of macrophage-derived cytokines, such as tumor necrosis factor (TNF), and increasing the permeability of endothelium [5,6,7]. Clinical studies have reported that oxidative stress may contribute not only to endothelial dysfunction, but also to coronary artery disease activity, increasing the risk of cardiovascular events in patients with coronary artery disease [8].…”

Section: Introductionmentioning

confidence: 99%

Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway

et al. 2016

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Abstract:Oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Salidroside (SAL), one of the main effective constituents of Rhodiola rosea, has been reported to suppress oxidative stress-induced cardiomyocyte injury and necrosis by promoting transcription of nuclear factor E2-related factor 2 (Nrf2)-regulated genes such as heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase (quinone1) (NQO1). However, it has not been indicated whether SAL might ameliorate endothelial injury induced by oxidative stress. Here, our study demonstrated that SAL might suppress HUVEC cell injury induced by oxidative stress through activating the Nrf2 signaling pathway. The results of our study indicated that SAL decreased the levels of intercellular reactive oxygen species (ROS) and malondialdehyde (MDA), and improved the activities of superoxide dismutase (SOD) and catalase (CAT), resulting in protective effects against oxidative stress-induced cell damage in HUVECs. It suppressed oxidative stress damage by inducing Nrf2 nuclear translocation and activating the expression of Nrf2-regulated antioxidant enzyme genes such as HO-1 and NQO1 in HUVECs. Knockdown of Nrf2 with siRNA abolished the cytoprotective effects against oxidative stress, decreased the expression of Nrf2, HO-1, and NQO1, and inhibited the nucleus translocation of Nrf2 in HUVECs. This study is the first to demonstrate that SAL suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway

et al. 2016

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“…Various environmental and intrinsic factors in the pathological process of AS, such as mechanical stress, radiation, reactive oxygen species or nitrogen mediators, lipids, and inflammatory cytokines can mediate ECs apoptosis and promote the development of AS lesions. Among them, ROS plays an important role in vascular physiology and pathology [19]. A low dose of ROS can be used as a signal molecule in ECs to upregulate redox regulator thioredoxin and have the effect of antiapoptosis, while a high concentration of ROS can promote ECs dysfunction and even apoptosis.…”

Section: Discussionmentioning

confidence: 99%

CD137 Signaling Promotes Endothelial Apoptosis by Inhibiting Nrf2 Pathway, and Upregulating NF-κB Pathway

Geng

Yang

Zhang

et al. 2020

Mediators of Inflammation

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Background. Endothelial dysfunction and apoptosis resulting from oxidative stress can lead to the development of atherosclerosis. Our group has previously showed that CD137 signaling contributes to the progression of atherosclerosis and the vulnerability of plaques. The aim of this study is to investigate the effects of CD137 signaling in atherosclerosis on endothelial cells (ECs) apoptosis and to explore the underlying mechanisms. Methods. Serum samples were collected from 11 patients with acute myocardial infarction and 4 controls. Peritoneal injection of agonist-CD137 recombinant protein in ApoE−/− mice was used to determine whether CD137 signaling can promote apoptosis in vivo, and human umbilical vein endothelial cells treated with agonist-CD137 recombinant protein, M5580 (a Nrf2 pathway agonist) and CAPE (a NF-κB pathway inhibitor) were used to explore the effect of Nrf2 and NF-κB pathway in CD137 signaling-induced ECs apoptosis in vitro. Results. ELISA showed that Bcl-2 in the serum of AMI patients was lower than that of the control group, while TNF-α and sCD137 were higher than that of the control group. Confocal microscopy and Western blot analysis showed that the nuclear translocation of Nrf2 in the agonist-CD137 group was significantly inhibited, and the expression of its downstream antioxidant enzymes was also decreased when compared with control. Immunofluorescence and Western blot results showed that the nuclear translocation of NF-κB in the agonist-CD137 group was enhanced, and ELISA results showed that the secretion of proinflammatory cytokines in the agonist-CD137 group was increased. Immunofluorescence results revealed that ROS production in the agonist-CD137 group was higher than that in control, M5580 (a Nrf2 pathway agonist) and CAPE (a NF-κB pathway inhibitor) groups. In vitro studies using HUVECs and in vivo studies using high-fat-fed ApoE−/− mice showed that the number of apoptotic endothelial cells was the highest in the agonist-CD137 group. By contrast, both M5580 and CAPE treatments were able to reduce CD137 induced ECs apoptosis. Conclusions. Our results showed that CD137 signaling promotes ECs apoptosis through prooxidative and proinflammatory mechanisms, mediated by Nrf2 and NF-κB pathways, respectively.

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“…When cellular ROS formation exceeds the capacity of antioxidant defenses, oxidative stress occurs. Excessive production of free radicals leads to oxidative damage in lipids, proteins, and especially DNA, which may trigger an apoptotic response and atherogenic process through cellular dysfunction [56] , [57] . An epidemiological investigation [58] showed that low-dose folic acid therapy can improve vascular function by altering oxidative stress in vessels.…”

Section: Discussionmentioning

confidence: 99%

Folic acid modulates VPO1 DNA methylation levels and alleviates oxidative stress-induced apoptosis in vivo and in vitro

Cui

et al. 2018

Redox Biology

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Endothelial cell injury and apoptosis play a primary role in the pathogenesis of atherosclerosis. Moreover, accumulating evidence indicates that oxidative injury is an important risk factor for endothelial cell damage. In addition, low folate levels are considered a contributing factor to promotion of vascular disease because of the deregulation of DNA methylation. We aimed to investigate the effects of folic acid on injuries induced by oxidative stress that occur via an epigenetic gene silencing mechanism in ApoE knockout mice fed a high-fat diet and in human umbilical vein endothelial cells treated with oxidized low-density lipoprotein (ox-LDL). We assessed how folic acid influenced the levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG, an oxidative DNA damage marker) and cellular apoptosis in in vivo and in vitro models. Furthermore, we analyzed DNA methyltransferase (DNMT) activity, vascular peroxidase 1 (VPO1) expression, and promoter methylation in human umbilical vein endothelial cells. Our data showed that folic acid reduced 8-OHdG levels and decreased apoptosis in the aortic tissue of ApoE−/− mice. Likewise, our in vitro experiments showed that folic acid protects against endothelial dysfunction induced by ox-LDL by reducing reactive oxygen species (ROS)-derived oxidative injuries, 8-OHdG content, and the apoptosis ratio. Importantly, this effect was indirectly caused by increased DNMT activity and altered DNA methylation at VPO1 promoters, as well as changes in the abundance of VPO1 expression. Collectively, we conclude that folic acid supplementation may prevent oxidative stress-induced apoptosis and suppresses ROS levels through downregulating VPO1 as a consequence of changes in DNA methylation, which may contribute to beneficial effects on endothelial function.

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Oxidatív stressz és atherosclerosis

Cited by 17 publications

References 11 publications

Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway

Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway

CD137 Signaling Promotes Endothelial Apoptosis by Inhibiting Nrf2 Pathway, and Upregulating NF-κB Pathway

Folic acid modulates VPO1 DNA methylation levels and alleviates oxidative stress-induced apoptosis in vivo and in vitro

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