scholarly journals Protective effects of Histidine-rich glycoprotein on human vascular endothelial cells

2018 ◽  
Vol WCP2018 (0) ◽  
pp. PO3-3-52
Author(s):  
Yuan Gao ◽  
Hidenori Wake ◽  
Keyue Liu ◽  
Kiyoshi Teshigawara ◽  
Shuji Mori ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Protective Effects

scholarly journals Resolvin D1 Reverts Lipopolysaccharide-Induced TJ Proteins Disruption and the Increase of Cellular Permeability by Regulating IκBαSignaling in Human Vascular Endothelial Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Xingcai Zhang ◽  
Tingting Wang ◽  
Ping Gui ◽  
Chengye Yao ◽  
Wei Sun ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Permeability ◽  
Vascular Endothelial Cells ◽  
Cell Permeability ◽  
Endothelial Barrier ◽  
Lipid Mediator ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Resolvin D1 ◽  
Cellular Permeability

Tight Junctions (TJ) are important components of paracellular pathways, and their destruction enhances vascular permeability. Resolvin D1 (RvD1) is a novel lipid mediator that has treatment effects on inflammatory diseases, but its effect on inflammation induced increase in vascular permeability is unclear. To understand whether RvD1 counteracts the lipopolysaccharide (LPS) induced increase in vascular cell permeability, we investigated the effects of RvD1 on endothelial barrier permeability and tight junction reorganization and expression in the presence or absence of LPS stimulation in cultured Human Vascular Endothelial Cells (HUVECs). Our results showed that RvD1 decreased LPS-induced increased in cellular permeability and inhibited the LPS-induced redistribution of zo-1, occludin, and F-actin in HUVECs. Moreover, RvD1 attenuated the expression of IκBαin LPS-induced HUVECs. The NF-κB inhibitor PDTC enhanced the protective effects of RvD1 on restoration of occludin rather than zo-1 expression in LPS-stimulated HUVECs. By contrast, the ERK1/2 inhibitor PD98059 had no effect on LPS-induced alterations in zo-1 and occludin protein expressions in HUVECs. Our data indicate that RvD1 protects against impairment of endothelial barrier function induced by LPS through upregulating the expression of TJ proteins in HUVECs, which involves the IκBαpathway but not the ERK1/2 signaling.

scholarly journals Sirt1 Inhibits Oxidative Stress in Vascular Endothelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Weijin Zhang ◽  
Qiaobing Huang ◽  
Zhenhua Zeng ◽  
Jie Wu ◽  
Yaoyuan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Protective Role ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Key Factor ◽  
Antioxidative Stress

The vascular endothelium is a layer of cells lining the inner surface of vessels, serving as a barrier that mediates microenvironment homeostasis. Deterioration of either the structure or function of endothelial cells (ECs) results in a variety of cardiovascular diseases. Previous studies have shown that reactive oxygen species (ROS) is a key factor that contributes to the impairment of ECs and the subsequent endothelial dysfunction. The longevity regulator Sirt1 is a NAD+-dependent deacetylase that has a potential antioxidative stress activity in vascular ECs. The mechanisms underlying the protective effects involve Sirt1/FOXOs, Sirt1/NF-κB, Sirt1/NOX, Sirt1/SOD, and Sirt1/eNOs pathways. In this review, we summarize the most recent reports in this field to recapitulate the potent mechanisms involving the protective role of Sirt1 in oxidative stress and to highlight the beneficial effects of Sirt1 on cardiovascular functions.

scholarly journals Protective Effect of Fenofibrate on Oxidative Stress-Induced Apoptosis in Retinal–Choroidal Vascular Endothelial Cells: Implication for Diabetic Retinopathy Treatment

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 712 ◽  
Author(s):  
Ying-Jung Hsu ◽  
Chao-Wen Lin ◽  
Sheng-Li Cho ◽  
Wei-Shiung Yang ◽  
Chung-May Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
B Cell ◽  
Cell Lymphoma ◽  
Vascular Endothelial Cells ◽  
B Cell Lymphoma ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Amino Terminal

Diabetic retinopathy (DR) is an important microvascular complication of diabetes and one of the leading causes of blindness in developed countries. Two large clinical studies showed that fenofibrate, a peroxisome proliferator-activated receptor type α (PPAR-α) agonist, reduces DR progression. We evaluated the protective effects of fenofibrate on retinal/choroidal vascular endothelial cells under oxidative stress and investigated the underlying mechanisms using RF/6A cells as the model system and paraquat (PQ) to induce oxidative stress. Pretreatment with fenofibrate suppressed reactive oxygen species (ROS) production, decreased cellular apoptosis, diminished the changes in the mitochondrial membrane potential, increased the mRNA levels of peroxiredoxin (Prx), thioredoxins (Trxs), B-cell lymphoma 2 (Bcl-2), and Bcl-xl, and reduced the level of B-cell lymphoma 2-associated X protein (Bax) in PQ-stimulated RF/6A cells. Western blot analysis revealed that fenofibrate repressed apoptosis through cytosolic and mitochondrial apoptosis signal-regulated kinase-1 (Ask)-Trx-related signaling pathways, including c-Jun amino-terminal kinase (JNK) phosphorylation, cytochrome c release, caspase 3 activation, and poly (ADP-ribose) polymerase-1 (PARP-1) cleavage. These protective effects of fenofibrate on RF/6A cells may be attributable to its anti-oxidative ability. Our research suggests that fenofibrate could serve as an effective adjunct therapy for ocular oxidative stress-related disorders, such as DR.

Cordycepin Attenuates Palmitic Acid-Induced Inflammation and Apoptosis of Vascular Endothelial Cells through Mediating PI3K/Akt/eNOS Signaling Pathway

2021 ◽  
pp. 1-20
Author(s):  
Chang-Wen Ku ◽  
Tsung-Jung Ho ◽  
Chih-Yang Huang ◽  
Pei-Ming Chu ◽  
Hsiu-Chung Ou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Palmitic Acid ◽  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Vascular Endothelial Cells ◽  
Cordyceps Sinensis ◽  
Ros Generation ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Anti Inflammatory

A well-known medicinal mushroom in the field of traditional Chinese medicine, Cordyceps sinensis, is a rare natural-occurring entomopathogenic fungus, and it typically grows at high altitudes on the plateau of the Himalayan. Previous studies indicated that cordycepin, the main bioactive chemical of Cordyceps sinensis, has very potent anticancer, anti-oxidant and anti-inflammatory activities. However, its protective effects against atherosclerotic changes in vascular endothelial cells have not been fully elucidated. In this study, we showed that pretreatment with cordycepin significantly attenuated palmitic acid (PA)-induced cytotoxicity, reactive oxygen species (ROS) generation, and inflammatory responses. We found that PA decreased phosphorylation of Akt, eNOS, and bioavailability of nitric oxide (NO), which in turn activated NF-[Formula: see text]B and the downstream inflammatory responses. All these detrimental events were markedly blocked by pretreatment with cordycepin. Moreover, cordycepin ameliorated destabilization of mitochondrial permeability, cytosolic calcium rises, and apoptotic features caused by PA. In addition, all these anti-inflammatory and anti-apoptosis effects of cordycepin were found to be inhibited by the PI3K and eNOS inhibitor, suggesting that its anti-atherosclerotic effects may partially be mediated by the PI3K/Akt/eNOS signaling pathway.

Effects of Ropivacaine Nanoparticles on the Apoptosis of Cerebral Vascular Endothelial Cells

2020 ◽  
Vol 20 (12) ◽  
pp. 7299-7304
Author(s):  
Duanyu Wang ◽  
Yajun Liu ◽  
Wei Liu ◽  
Haiyan Qi
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Saline Control ◽  
Sham Operation ◽  
Apoptotic Cells ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Male Wistar Rats ◽  
Ischemic Brain Edema ◽  
Capillary Endothelial Cells

To investigate the protective effect of ropivacaine nanoparticles on endothelial cells in the blood brain barrier (BBB) during the development of ischemic brain edema, and its effects on endothelial cell death. Forty-two male Wistar rats weighing 250–300 g and aged 3–4 months were randomly divided into three groups: (1) ropivacaine nanoparticles, (2) saline control and (3) sham operation groups. The membrane of capillary endothelial cells in the animals treated with ropivacaine nanoparticles were intact, with reduced edema, and less severe brain injury when compared to the control. In the ropivacaine nanoparticle group, the number of apoptotic cells decreased at 6 h and 24 h after ischemia, while the number of apoptotic cells in the ischemic penumbra increased. The number of apoptotic cells in the ropivacaine nanoparticles group was significantly lower than in the saline treated control. Ropivacaine nanoparticles exert significant protective effects on the vascular endothelial cells and the BBB during cerebral ischemia.

The Protective Effects of Propofol on Vascular Endothelial Cells

2002 ◽  
Vol 96 (Sup 2) ◽  
pp. A58
Author(s):  
Zhiyong Peng ◽  
Min Luo ◽  
Shiqiao Ye ◽  
Gavin Joynt ◽  
Lester Critchley
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Protective Effects

scholarly journals Genistein Acutely Stimulates Nitric Oxide Synthesis in Vascular Endothelial Cells by a Cyclic Adenosine 5′-Monophosphate-Dependent Mechanism

Endocrinology ◽  
2004 ◽  
Vol 145 (12) ◽  
pp. 5532-5539 ◽  
Author(s):  
Dongmin Liu ◽  
Laurie L. Homan ◽  
Joseph S. Dillon
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Vascular Function ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Nitric Oxide Synthesis ◽  
Enos Activity ◽  
Endothelial Nitric Oxide

Abstract Genistein may improve vascular function, but the mechanism of this effect is unclear. We tested the hypothesis that genistein directly regulates vascular function through stimulation of endothelial nitric oxide synthesis. Genistein activated endothelial nitric oxide synthase (eNOS) in intact bovine aortic endothelial cells and human umbilical vein endothelial cells over an incubation period of 10 min. The maximal eNOS activity was at 1 μm genistein. Consistent with this activation pattern, 1 μm genistein maximally stimulated the phosphorylation of eNOS at serine 1179 at 10 min of incubation. The rapid activation of eNOS by genistein was not dependent on RNA transcription or new protein synthesis and was not blocked by a specific estrogen receptor antagonist. In addition, inhibition of MAPK or phosphatidylinositol 3-OH kinase/Akt kinase had no affect on eNOS activation by genistein. Furthermore, the genistein effect on eNOS was also independent of tyrosine kinase inhibition. However, inhibition of cAMP-dependent kinase [protein kinase A (PKA)] by H89 completely abolished the genistein-stimulated eNOS activation and phosphorylation, suggesting that genistein acted through a PKA-dependent pathway. These findings demonstrated that genistein had direct nongenomic effects on eNOS activity in vascular endothelial cells, leading to eNOS activation and nitric oxide synthesis. These effects were mediated by PKA and were unrelated to an estrogenic effect. This cellular mechanism may underlie some of the cardiovascular protective effects proposed for soy phytoestrogens.

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