scholarly journals GW26-e2215 Effects of Atorvastatin on JNK/AP-1 Signaling Pathway and the Expression of Related Factors in high glucose concentration-induced Vascular Endothelial Cells

2015 ◽  
Vol 66 (16) ◽  
pp. C90
Author(s):  
Fanghui Chen
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
High Glucose ◽  
Glucose Concentration ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
High Glucose Concentration ◽  
Related Factors

Resveratrol inhibits high-glucose-induced inflammatory “metabolic memory” in human retinal vascular endothelial cells through SIRT1-dependent signaling

2019 ◽  
Vol 97 (12) ◽  
pp. 1141-1151 ◽  
Author(s):  
Tingting Jiang ◽  
Junxiang Gu ◽  
Wenwen Chen ◽  
Qing Chang
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Cytokines ◽  
High Glucose ◽  
Glucose Concentration ◽  
Vascular Endothelial Cells ◽  
Sirtuin 1 ◽  
Metabolic Memory ◽  
Vascular Endothelial ◽  
High Glucose Concentration ◽  
Compound C

Diabetes induces vascular endothelial damage and this study investigated high-glucose-induced inflammation “metabolic memory” of human retinal vascular endothelial cells (HRVECs), the effects of resveratrol on HRVECs, and the underlying signaling. HRVECs were grown under various conditions and assayed for levels of sirtuin 1 (SIRT1); acetylated nuclear factor κB (Ac-NF-κB); NOD-like receptor family, pyrin domain containing 3 (NLRP3); and other inflammatory cytokines; and cell viability. A high glucose concentration induced HRVEC inflammation metabolic memory by decreasing SIRT1 and increasing Ac-NF-κB, NLRP3, caspase 1, interleukin-1β, inducible nitric oxide synthase, and tumor necrosis factor α, whereas exposure of HRVECs to a high glucose medium for 4 days, followed by a normal glucose concentration for an additional 4 days, failed to reverse these changes. A high glucose concentration also significantly reduced HRVEC viability. In contrast, resveratrol, a selective SIRT1 activator, markedly enhanced HRVEC viability and reduced the inflammatory cytokines expressions. In addition, high glucose reduced AMP-activated protein kinase (AMPK) phosphorylation and retained during the 4 days of the reversal period of culture. The effects of resveratrol were abrogated after co-treatment with the SIRT1 inhibitor nicotinamide and the AMPK inhibitor compound C. In conclusion, resveratrol was able to reverse high-glucose-induced inflammation “metabolic memory” of HRVECs by activation of the SIRT1/AMPK/NF-κB pathway.

scholarly journals Curcumin suppresses oxidative stress via regulation of ROS/NF-κB signaling pathway to protect retinal vascular endothelial cell in diabetic retinopathy

2020 ◽  
Author(s):  
Jiang Huang ◽  
Quanyong Yi ◽  
Yao Chen ◽  
Yi Li ◽  
Guoxu Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Flow Cytometry ◽  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
High Glucose ◽  
Glucose Concentration ◽  
Vascular Endothelial Cells ◽  
Control Group ◽  
Vascular Endothelial ◽  
High Glucose Concentration

Abstract Background: Diabetic retinopathy (DR) is one of the most serious complications of diabetes mellitus and a leading blindness disease in the world. The retinal vascular endothelial cells can be damaged by oxidative stress even in the early stage of diabetic retinopathy. NF-κB is a key transcription factor in cell apoptosis and oxidative stress. Curcumin can relieve oxidative stress induced by high glucose. This study aimed to investigate the effect of curcumin on the rat retinal vascular endothelial cells (RRVECs) in DR and to deduce the possible molecular mechanism. Methods: The cultured RRVECs were identified by both of vWF and CD31 expression.The RRVECs were divided into four groups: the normal control group, the osmolarity control group, the high glucose group and the curcumin treatment group (High glucose +Curcumin). We observed the different morphological changes in the groups by transmission electron microscopy. Oxidative stress was detected by flow cytometry. The Activation of ROS/NF-κB signal pathway was detected by electrophoretic Mobility Shift Assay (EMSA), immunohistochemistry and western-blot; the apoptosis of RRVECs was tested by flow cytometry. Results: We found that curcumin reduced the reactive oxygen species (ROS) and relieved the apoptosis in RRVECs exposed to the high glucose by flow cytometry. We detected that the increased activity of NF-κB and phosphorylated NF-κB in RRVECs induced by high glucose concentration was significantly suppressed by curcumin. Furthermore, based on the assay quantifying the level of apoptosis-related proteins, including bcl-2 and bax, we illustrated that curcumin could decrease the apoptosis of RRVECs induced by high glucose concentration. Conclusion: We concluded that ROS/NF-κB signaling pathway played an important role in the progress of DR and curcumin could suppress the oxidative stress via regulation of NF-κB signal to protect the RRVECs in DR.

Schisandrin B ameliorates high-glucose-induced vascular endothelial cells injury by regulating the Noxa/Hsp27/NF-κB signaling pathway

2019 ◽  
Vol 97 (6) ◽  
pp. 681-692 ◽  
Author(s):  
Qiu-Ning Lin ◽  
Yong-Dong Liu ◽  
Si-En Guo ◽  
Rui Zhou ◽  
Qun Huang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
High Glucose ◽  
Vascular Endothelial Cells ◽  
Schisandrin B ◽  
Vascular Endothelial ◽  
Inflammatory Cascade ◽  
Tnf Α ◽  
Anti Inflammation

Background: To address the molecular mechanism of the anti-inflammation effects of schisandrin B (Sch B) in atherosclerosis, we examined injured HMEC-1, HBMEC, and HUVEC-12 cells induced by high glucose (HG). Methods: Western blot was performed to detect the levels of the proteins Hsp27, Noxa, TLR5, p-IκBα, and p-p65 in HG-induced cells, while ELISA was used to analyze the inflammatory cytokines TNF-α, IL-6, MCP-1, and IL-1β in cells with Hsp27 or Noxa stable expression. Results: Overexpression of Hsp27 upregulated the inflammatory cytokines and the release of IκBα, promoted transportation of p65 into the nucleus, and lastly, affected the inflammation process, while Sch B counteracted the upregulation. In addition, the effect of Noxa overexpression, which is different from Hsp27 overexpression, was consistent with that of Sch B treatment. Conclusions: Sch B may inhibit the inflammatory cascade and alleviate the injury to HMEC-1, HBMEC, and HUEVC-12 cells caused by HG by regulating the Noxa/Hsp27/NF-κB signaling pathway.

scholarly journals Sulodexide reduces glucose induced senescence in human retinal endothelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
A. Gericke ◽  
K. Suminska-Jasińska ◽  
A. Bręborowicz
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Glucose Concentration ◽  
Chronic Exposure ◽  
Replicative Senescence ◽  
Population Doubling ◽  
Population Doubling Time ◽  
High Glucose Concentration ◽  
Retinal Endothelial Cells

AbstractChronic exposure of retinal endothelium cells to hyperglycemia is the leading cause of diabetic retinopathy. We evaluated the effect of high glucose concentration on senescence in human retinal endothelial cells (HREC) and modulation of that effect by Sulodexide. Experiments were performed on HREC undergoing in vitro replicative senescence in standard medium or medium supplemented with glucose 20 mmol/L (GLU) or mannitol 20 mnol/L (MAN). Effect of Sulodexide 0.5 LRU/mL (SUL) on the process of HREC senescence was studied. Glucose 20 mmol/L accelerates senescence of HREC: population doubling time (+ 58%, p < 0.001) β-galactosidase activity (+ 60%, p < 0.002) intracellular oxidative stress (+ 65%, p < 0.01), expression of p53 gene (+ 118%, p < 0.001). Senescent HREC had also reduced transendothelial electrical resistance (TEER) (− 30%, p < 0.001). Mannitol 20 mmol/L used in the same scenario as glucose did not induce HREC senescence. In HREC exposed to GLU and SUL, the senescent changes were smaller. HREC, which became senescent in the presence of GLU, demonstrated higher expression of genes regulating the synthesis of Il6 and VEGF-A, which was reflected by increased secretion of these cytokines (IL6 + 125%, p < 0.001 vs control and VEGF-A + 124% p < 0.001 vs control). These effects were smaller in the presence of SUL, and additionally, an increase of TEER in the senescent HREC was observed. Chronic exposure of HREC to high glucose concentration in medium accelerates their senescence, and that process is reduced when the cells are simultaneously exposed to Sulodexide. Additionally, Sulodexide decreases the secretion of IL6 and VEGF-A from senescent HREC and increases their TEER.

Scutellarin ameliorates high glucose-induced vascular endothelial cells injury by activating PINK1/Parkin-mediated mitophagy

2021 ◽  
Vol 271 ◽  
pp. 113855
Author(s):  
Junxiao Xi ◽  
Yuezhao Rong ◽  
Zifeng Zhao ◽  
Yihai Huang ◽  
Pu Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial
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