The Effect of N-Methyl-2-Pyridone-5-Carboxamide - A Nicotinamide Catabolite on Poly ADP-Rybosylation and Oxidative Stress Injury in Endothelial Cells

2005 ◽  
Vol 24 (4) ◽  
pp. 259-262
Author(s):  
E. M. Slominska ◽  
R. T. Smolenski ◽  
F. Osborne ◽  
J. Swierczynski ◽  
M. H. Yacoub
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
And Oxidative Stress

scholarly journals Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Haijun Zhao ◽  
Yanhui He
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Inflammatory Response ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Marrow Mesenchymal Stem Cells ◽  
And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

scholarly journals Puerarin Attenuates LPS-Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Xing Chang ◽  
Tian Zhang ◽  
Dong Liu ◽  
Qingyan Meng ◽  
Peizheng Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Quality Control ◽  
Endothelial Cells ◽  
Protective Effect ◽  
Umbilical Vein ◽  
Mitochondrial Quality Control ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Umbilical Vein Endothelial Cells ◽  
And Oxidative Stress

Atherosclerosis is closely associated with the inflammatory reaction of vascular endothelial cells. Puerarin (Pue), the main active component isolated from the rhizome of Pueraria lobata, is an isoflavone compound with potent antioxidant properties. Although Pue exhibits promising antiatherosclerotic pharmacological effects, only a few studies have reported its protective effect on endothelial cells. This study found that Pue could partly regulate mitochondrial function in human umbilical vein endothelial cells (HUVECs) and reduce or inhibit lipopolysaccharide-induced inflammatory reactions and oxidative stress injury in HUVECs, likely via mitochondrial quality control. Furthermore, the protective effect of Pue on HUVECs was closely related to the SIRT-1 signaling pathway. Pue increased autophagy and mitochondrial antioxidant potential via increased SIRT-1 expression, reducing excessive production of ROS and inhibiting the expression of inflammatory factors and oxidative stress injury. Therefore, Pue may improve mitochondrial respiratory function and energy metabolism, increasing the vulnerability of HUVECs to an inflammatory state.

Effects of Atorvastatin Combined with Nano-Selenium on Blood Lipids and Oxidative Stress in Atherosclerotic Rats

2021 ◽  
Vol 21 (2) ◽  
pp. 1331-1337
Author(s):  
Zhe Han ◽  
Yang Wang ◽  
Jing Li
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Endothelial Cell ◽  
High Efficiency ◽  
Biological Effects ◽  
Lipid Lowering ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Combined Use ◽  
And Oxidative Stress

Dyslipidemia and oxidative stress injury of blood vessel walls play important roles in the formation of atherosclerosis (AS) and plaque progression. This is also the main pathological basis for atherosclerosis. Statins, as inhibitors of HMG-CoA reductase in the process of cholesterol biosynthesis, have become key drugs for lipid-lowering treatment. Many studies have found the anti-atherosclerotic effect of atorvastatin is far beyond the lipid-lowering effect. Its lipid-lowering effects are also involved, such as anti-inflammatory, inhibiting endothelial cell ROS production, and improving endothelial cell damage. Nano selenium (Nano-Se) shows stronger anti-oxidation ability, lower toxicity, high efficiency absorption and strong immune regulation ability. Because of the unique biological effects of Nano-Se, it has broad prospects in the field of human health care. Therefore, in this study, by constructing a rat model of abnormal lipid metabolism, we observed changes in parameters such as serum peroxidase (MPO), propylene glycol (MDA), superoxide dismutase (SOD), and blood lipid levels in atherosclerotic rats Happening, furthermore, the effects of atorvastatin+nano-selenium on lipid metabolism disorders and the protective effects and mechanisms of oxidative stress injury in rats were investigated and with a view to providing new targets for the treatment of arteriosclerosis. The results of this study demonstrated that contrast to the AS rat, the combined use of atorvastatin+nano-selenium group could significantly reduce serum TC, TG, and LDL-C contents, and declined tissue lesions such as aortic arch and liver; Significantly enhanced the activities of GPx-1 and SOD in serum, decreased MDA content, and increased the SOD activity in rat aorta. These results suggested that the combined use of atorvastatin+nano-selenium has good protection against oxidative stress caused by disorders of lipid metabolism.

Alginate oligosaccharide protects endothelial cells against oxidative stress injury via integrin-α/FAK/PI3K signaling

2020 ◽  
Vol 42 (12) ◽  
pp. 2749-2758
Author(s):  
Jing Zhao ◽  
Yue Han ◽  
Zongqiu Wang ◽  
Rui Zhang ◽  
Guimei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Pi3k Signaling ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Alginate Oligosaccharide

scholarly journals Fermented Chinese Formula Shuan-Tong-Ling Protects Brain Microvascular Endothelial Cells against Oxidative Stress Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Lingjing Tan ◽  
Xiang Zhang ◽  
Zhigang Mei ◽  
Jinfeng Wang ◽  
Xiaoli Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Endothelial Cells ◽  
Cell Senescence ◽  
Microvascular Endothelial Cells ◽  
Dependent Manner ◽  
Brain Microvascular Endothelial Cells ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Microvascular Endothelial

Fermented Chinese formulaShuan-Tong-Ling(STL), composed of fourteen medicinal herbs, was an experiential formula by Dr. Zhigang Mei for treating vascular encephalopathy, but the underlying mechanisms remained unknown. In this study, we aimed to investigate the protective effects of fermented STL on hydrogen peroxide- (H2O2-) induced injury in rat brain microvascular endothelial cells (BMECs) and the possible mechanisms. Cultured BMECs were treated with H2O2, STL, or nicotinamide (NAM, a SIRT1 inhibitor). Then, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was employed to detect cell proliferation and senescence-associated beta-galactosidase (SA-β-gal) was used to examine cell senescence. Cell nuclei were observed by 4′,6-diamidino-2-phenylindole. Additionally, changes in reactive oxygen species (ROS), superoxide dismutase (SOD), and glutathione (GSH) levels were measured. Expression of SIRT1, p21, and PGC-1αwas determined by western blot. Cell proliferation significantly increased with STL treatment in a dose-dependent manner. H2O2treatment could intensify cell senescence and nuclei splitting or pyknosis. With STL treatment, the reduced ROS level was accompanied by increased SOD and GSH activity. Further assays showed upregulation of SIRT1 and PGC-1αand downregulation of p21 after STL treatment. The results revealed that STL could protect BMECs against oxidative stress injury at least partially through the SIRT1 pathway.

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