scholarly journals Anti‐Inflammatory Effects of Quercetin on High‐Glucose and Pro‐Inflammatory Cytokine Challenged Vascular Endothelial Cell Metabolism

2021 ◽  
pp. 2000777
Author(s):  
Besim Ozyel ◽  
Gwénaëlle Le Gall ◽  
Paul W. Needs ◽  
Paul A. Kroon
Keyword(s):  
Endothelial Cell ◽  
High Glucose ◽  
Inflammatory Cytokine ◽  
Cell Metabolism ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Anti Inflammatory ◽  
Endothelial Cell Metabolism

scholarly journals OR14-06 Inhibition of Protein Kinase C-beta2 Phosphorylation Restores Nuclear Factor-Kappa B Activation and Improves Peripheral Arterial Disease in Diabetes

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Satyanarayana Alleboina ◽  
Madhu V Singh ◽  
Thomas Wong ◽  
Ayotunde Dokun
Keyword(s):  
Endothelial Cell ◽  
High Glucose ◽  
Hind Limb ◽  
Prolonged Exposure ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Human Vascular Endothelial Cell ◽  
Normal Glucose ◽  
Akita Mice

Abstract Peripheral artery disease (PAD) is atherosclerotic occlusion of vessel outside the heart and most commonly affects the lower extremities. Diabetes (DM) accelerates the course and severity of PAD. Studies have shown that vascular endothelial cell NF-κB activity is required for post ischemic adaptation in experimental PAD. To better understand how DM contributes to PAD severity, we investigated the role of DM hyperglycemia in the activation of NF-κB under ischemic conditions. Induced ischemia in human vascular endothelial cell (HUVEC) cultures increased components of both canonical and non-canonical NF-κB pathways in the nucleus (p65 1.0 ± 0.1 vs 1.5 ± 0.2, p< 0.05, RelB 1.0 ± 0.1 vs 1.5 ± 0.2, p<0.01). Similarly, HUVEC acutely exposed to high glucose (HG, 25 mM) activated both canonical (IκB-α degradation, normal vs. HG 1.25 ± 0.02 vs 0.9 ± 0.0, p<0.05) and non-canonical NF-κB (p100 degradation, normal vs HG 0.021±0.001 vs 0.016±0.000, p<0.05) pathways. Prolonged exposure (3 days) of HUVEC to high glucose before ischemia resulted in impaired NF-κB activation as evident from decreased IκB phosphorylation (pIκB/IκB in normal glucose and ischemia 1.56 ± 0.22 vs 1.12 ± 0.35, p<0.01). To understand the signaling pathways underlying the ischemic activation of the NF-κB pathway, we used an array of antibodies to phosphoproteins involved in the inflammatory pathway. Compared to the lysates from cells grown in normal glucose, the lysates from cells grown in prolonged high glucose had dramatically increased phosphorylation of PKC-β2 (PKC-β2pSer661, 8-fold increase). To test whether this increase in PKC-β2pSer66 impairs NF-κB activation by ischemia, we treated HUVECS with prolonged high glucose exposure and ruboxystaurin (Rbx) (20 nM), an inhibitor of PKC-β2 phosphorylation, prior to ischemic exposure. Immunoblotting results confirmed that inhibition of PKC-β2 phosphorylation enhanced the ischemia induced NF-κB activation in HUVEC in this condition. We then tested the effect of Rbx on PKC-β2 phosphorylation and NF-κB activation in vivo in Akita mice, a model for type 1 diabetes. Consistent with our in vitro findings, in experimental PAD, NF-κB activity in the ischemic hind limb of Akita mice was significantly lower than those of the wild type (WT) mice as measured by IκB-α degradation (WT ischemic vs Akita ischemic; 0.04 ± 0.03 vs 0.10 ± 0.04 p<0.05). However, treatment of Akita mice with Rbx increased NF-κB activation in the ischemic hind limb (Akita ischemic 0.10 ± 0.04 vs ischemic+ Rbx 0.05 ± 0.02, p<0.05). Moreover, compared to the WT mice, the untreated Akita mice showed an impaired perfusion in the ischemic limbs (% perfusion recovery, WT vs Akita; 80.1 ± 10.3 vs 55.7 ± 10.1, p<0.05, n=5-8) that was improved in Rbx treated Akita mice (96.3 ± 2.3, p<0.01). Thus, hyperglycemic conditions increase PKC-β2pSer66 in endothelial cells attenuating salutary NF-κB activation contributing to poor PAD outcomes in DM.

scholarly journals Antioxidant and Anti-Inflammatory Effects of Blueberry Anthocyanins on High Glucose-Induced Human Retinal Capillary Endothelial Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Wuyang Huang ◽  
Zheng Yan ◽  
Dajing Li ◽  
Yanhong Ma ◽  
Jianzhong Zhou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Vascular Endothelial Cell ◽  
Intercellular Adhesion Molecule ◽  
Vascular Endothelial ◽  
Intercellular Adhesion Molecule 1 ◽  
Eye Health ◽  
Retinal Capillary ◽  
Capillary Endothelial Cells ◽  
Anti Inflammatory

Blueberries possess abundant anthocyanins, which benefit eye health. The purpose of this study was to explore the protective functional role of blueberry anthocyanin extract (BAE) and its predominant constituents, malvidin (Mv), malvidin-3-glucoside (Mv-3-glc), and malvidin-3-galactoside (Mv-3-gal), on high glucose- (HG-) induced injury in human retinal capillary endothelial cells (HRCECs). The results showed that BAE, Mv, Mv-3-glc, and Mv-3-gal enhanced cell viability (P<0.05 versus the HG group at 24 h); decreased the reactive oxygen species (ROS, P<0.01 versus the HG group both at 24 and 48 h); and increased the enzyme activity of catalase (CAT) and superoxide dismutase (SOD) (P<0.05 versus the HG group both at 24 and 48 h). Mv could greatly inhibit HG-induced Nox4 expression both at 24 and 48 h (P<0.05), while BAE and Mv-3-gal downregulated Nox4 only at 48 h (P<0.05). Mv, Mv-3-glc, and Mv-3-gal also changed nitric oxide (NO) levels (P<0.05). BAE and Mv-3-glc also influenced angiogenesis by decreasing the vascular endothelial cell growth factor (VEGF) level and inhibiting Akt pathway (P<0.05). Moreover, Mv and Mv-3-glc inhibited HG-induced intercellular adhesion molecule-1 (ICAM-1, P<0.001) and nuclear factor-kappa B (NF-κB) (P<0.05). It indicated that blueberry anthocyanins protected HRCECs via antioxidant and anti-inflammatory mechanisms, which could be promising molecules for the development of nutraceuticals to prevent diabetic retinopathy.

scholarly journals Antioxidant and Anti-inflammatory Protective Properties of Thai Shallot (Allium ascalonicum cv. Chiangmai) Juice on Human Vascular Endothelial Cell Lines (EA.hy926)

2019 ◽  
Vol 16 (3) ◽  
pp. 175-184
Author(s):  
Sakaewan OUNJAIJEAN ◽  
Sukanya CHACHIYO ◽  
Kanokwan KULPRACHAKARN ◽  
Kongsak BOONYAPRANAI ◽  
Somdet SRICHAIRATANAKOOL ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Membrane Lipid ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Ros Production ◽  
Food Ingredient ◽  
Human Vascular Endothelial Cell ◽  
Anti Inflammatory

Oxidative stress and inflammation are 2 major contributors to numerous life-threatening disorders, including vascular pathologies. Shallots (Allium ascalonicum) are a type of red onion which grows in Southeast Asia. Bulbs of this plant are used both as a food ingredient and in traditional medicine. This study attempted to investigate the possible ways that juice extracted from Thai shallot (A.ascalonicum cv. Chiangmai) bulbs could be used in the prevention of cardiovascular complications. The antioxidative and anti-inflammatory effects of shallot juice extract (SHE) on human vascular endothelial cells (EA.hy926) were investigated. Cell viability was evaluated by MTT assay, membrane lipid peroxidation by thiobarbituric acid reactive substances assay, intracellular reactive oxygen species (ROS) production by the fluorescent probe 6-carboxy-2'-7'-dichlorofluoresceine, and interleukin-6 (IL-6) released by ELISA. The shallot juice showed extremely low cytotoxicity against EA.hy926 cells, with IC50 of 41.9 and 27.3 mg/ml for 24 h- and 48 h-incubation, respectively. SHE reduced the iron-induced malondialdehyde production in a dose-dependent manner. The extract also demonstrated antioxidant activity as shown by a significant reduction of H2O2-induced ROS production at a low concentration (< 200 mg/ml). Furthermore, SHE significantly attenuated the level of IL-6 released during lipopolysaccharide stimulation (p < 0.05). It is of interest that the juice extracted from Thai shallot bulbs demonstrated both cellular antioxidant and anti-inflammatory properties in endothelial cell models, combined with a reduction in toxicity. Shallot extract could be considered as a nutraceutical for the prevention or management of vascular diseases as it is related to oxidative stress and inflammation.

scholarly journals The effect and action mechanism of resveratrol on the vascular endothelial cell by high glucose treatment

2016 ◽  
Vol 23 (1) ◽  
pp. S16-S21 ◽  
Author(s):  
Xun Liu ◽  
Jie Tian ◽  
Quanhao Bai ◽  
Muhammad Aqeel Ashraf ◽  
Maliha Sarfraz ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
High Glucose ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Action Mechanism ◽  
Glucose Treatment

scholarly journals Resveratrol Attenuates High Glucose-Induced Vascular Endothelial Cell Injury by Activating the E2F3 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Xiaolian Ding ◽  
Wei Yao ◽  
Jie Zhu ◽  
Kaida Mu ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Endothelial Cell ◽  
High Glucose ◽  
Cell Injury ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Macrovascular Disease ◽  
Endothelial Injury ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury

Type 2 diabetes mellitus (T2DM) is the most common metabolic disease. High glucose-induced macrovascular disease and microangiopathy are major complications of diabetes. E2F3, a member of the E2F transcription factor family, is closely related to cardiovascular diseases. Resveratrol, a nonflavonoid polyphenolic compound widely found in plants, has been shown to have cardiovascular protection. However, there are few studies on whether resveratrol can effectively treat diabetic angiopathy, and the specific mechanism involved needs further study. This study investigated whether E2F3 transcription factors are involved in the process of vascular endothelial injury induced by high glucose and observed its effects on the proliferation of vascular endothelial cells. Then, it analyzed whether resveratrol can inhibit high glucose-induced vascular endothelial cell injury by regulating the E2F3 pathway. We demonstrated that the expression level of the E2F3 transcription factor was significantly inhibited in high glucose state. Resveratrol inhibited high glucose-induced vascular endothelial cell injury by upregulating the E2F3 pathway. High glucose can induce vascular endothelial injury by inhibiting E2F3 gene expression, while resveratrol can inhibit high glucose-induced vascular endothelial injury by activating the E2F3 pathway.

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