Protective effects of 7-difluoromethyl-5,4′-dimethoxygenistein against human aorta endothelial injury caused by lysophosphatidyl choline

2011 ◽  
Vol 363 (1-2) ◽  
pp. 147-155 ◽  
Author(s):  
Fei Liu ◽  
Jian-Guo Cao ◽  
Cheng Li ◽  
Jin-Seng Tan ◽  
Xiao-Hua Fu
Keyword(s):  
Endothelial Injury ◽  
Human Aorta ◽  
Protective Effects ◽  
Lysophosphatidyl Choline

scholarly journals α -Lipoic Acid-Plus Ameliorates Endothelial Injury via Inhibiting the Apoptosis Pathway Mediated by Intralysosomal Cathepsins in Vivo and Vitro Endothelial Injury Model

2021 ◽  
Author(s):  
Yang Wang ◽  
Xiangqian Kong ◽  
Dejun Bao ◽  
Bin xu ◽  
Yongfei Dong ◽  
...  
Keyword(s):  
Cathepsin B ◽  
Caspase 3 ◽  
Endothelial Injury ◽  
Protective Effects ◽  
Apoptosis Pathway ◽  
Protein Levels ◽  
Oxidative Stress Level ◽  
Intimal Injury

Abstract PurposeWe tried to explore the potential role of the α-Lipoic acid-plus (LAP) in endothelial injury in vitro and vivo models. Simultaneously, possible endovascular protective mechanisms of LAP were also investigated further. MethodsIn vitro, oxyhemoglobin (OxyHb) stimulating human umbilical vein endothelial cells (HUVECs) simulated intimal injury. In vivo, carotid artery angioplasty injury was used to generate a model of rat carotid artery intimal injury (CAII). HUVECs and rats were treated with desferrioxamine (DFO) and LAP. ResultsIn experiment 1, we found that the expressions of Cathepsin B/D in endothelial tissue increased and reached peak point in 48 hours post rat CAII. In experiment 2, firstly, the protein levels of Cathepsin B/D, cleaved-caspase-3, Bax, Ferritin, Transferrin Receptor (TfR) markedly increased after CAII and reversed by DFO and LAP treatments. Besides, DFO and LAP treatments also reduced oxidative stress level and endothelial cells (ECs) necrosis of the damaged endometrium. In experiment 3, firstly, the protein levels of Cathepsin B/D, cleaved-caspase-3, Bax, Ferritin and TfR apparently increased post OxyHb stimulation, which were further aggravated by the addition of iron and decreased by DFO and LAP treatments. Moreover, DFO and LAP significantly ameliorated oxidative stress level, HUVECs injury, iron level, mitochondrial damage and were beneficial to maintain lysosomal integrity. Finally, LAP may have exerted more significant endovascular protective effects than DFO.ConclusionsLAP probably exerted endovascular protective effects via inhibiting the apoptosis pathway mediated by intralysosomal Cathepsins by chelating excessive iron in endothelial lysosomes post intimal injury.

scholarly journals Protective Effects of Total Flavones ofElaeagnus rhamnoides(L.) A. Nelson against Vascular Endothelial Injury in Blood Stasis Model Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Zhicheng Wei ◽  
Fang Zuo ◽  
Wenqian Wang ◽  
Li Wang ◽  
Dong Tong ◽  
...  
Keyword(s):  
Rat Model ◽  
Caspase 3 ◽  
Blood Stasis ◽  
Endothelial Injury ◽  
Water Bath ◽  
High Dose ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Von Willebrand ◽  
Ice Water

The aim was to evaluate the protective effects of total flavones ofElaeagnus rhamnoides(L.) A. Nelson (TFE) against vascular endothelial injury in blood stasis model rats and explore the potential mechanisms preliminarily. The model of blood stasis rat model with vascular endothelial injury was induced by subcutaneous injection of adrenaline combined with ice-water bath. Whole blood viscosity (WBV), histological examination, and prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen (FIB) were measured. Meanwhile, the levels of Thromboxane B2 (TXB2), 6-keto-PGF1α, von Willebrand factor (vWF), and thrombomodulin (TM) were detected. In addition, Quantitative Real-Time PCR (qPCR) was performed to identify PI3K, Erk2, Bcl-2, and caspase-3 gene expression. The results showed that TFE can relieve WBV, increase PT and APTT, and decrease FIB content obviously. Moreover, TFE might significantly downregulate the levels of TXB2, vWF, and TM in plasma and upregulate the level of 6-keto-PGF1αin plasma. Expressions of PI3K and Bcl-2 were increased and the expression of caspase-3 was decreased by TFE pretreatment in the rat model. Consequently, the study suggested that TFE may have the potential against vascular endothelial injury in blood stasis model rats induced by a high dose of adrenaline with ice-water bath.

scholarly journals In Vitro Vascular-Protective Effects of a Tilapia By-Product Oligopeptide on Angiotensin II-Induced Hypertensive Endothelial Injury in HUVEC by Nrf2/NF-κB Pathways

Marine Drugs ◽  
2019 ◽  
Vol 17 (7) ◽  
pp. 431 ◽  
Author(s):  
Jiali Chen ◽  
Fang Gong ◽  
Mei-Fang Chen ◽  
Chengyong Li ◽  
Pengzhi Hong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Umbilical Vein ◽  
Endothelial Injury ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Protective Effects ◽  
Ang Ii

Angiotensin II (Ang II) is closely involved in endothelial injury during the development of hypertension. In this study, the protective effects of the tilapia by-product oligopeptide Leu-Ser-Gly-Tyr-Gly-Pro (LSGYGP) on oxidative stress and endothelial injury in Angiotensin II (Ang II)-stimulated human umbilical vein endothelial cells (HUVEC) were evaluated. LSGYGP dose-dependently suppressed the fluorescence intensities of nitric oxide (NO) and reactive oxygen species (ROS), inhibited the nuclear factor-kappa B (NF-κB) pathway, and reduced inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and endothelin-1 (ET-1) expression, as shown by western blot. In addition, it attenuated the expression of gamma-glutamyltransferase (GGT) and heme oxygenase 1 (HO-1), as well as increasing superoxide dismutase (SOD) and glutathione (GSH) expression through the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Other experiments revealed that LSGYGP increased the apoptotic inhibition ratio between cleaved-caspase-3/procaspase-3, reduced expressions of pro-apoptotic ratio between Bcl-2/Bax, inhibited phosphorylation of mitogen-activated protein kinases (MAPK), and increased phosphorylation of the serine/threonine kinase (Akt) pathway. Furthermore, LSGYGP significantly decreased Ang II-induced DNA damage in a comet assay, and molecular docking results showed that the steady interaction between LSGYGP with NF-κB may be attributed to hydrogen bonds. These results suggest that this oligopeptide is effective in protecting against Ang II-induced HUVEC injury through the reduction of oxidative stress and alleviating endothelial damage. Thus, it has the potential for the therapeutic treatment of hypertension-associated diseases.

Protective effects of farrerol against hydrogen-peroxide-induced apoptosis in human endothelium-derived EA.hy926 cells

2013 ◽  
Vol 91 (9) ◽  
pp. 733-740 ◽  
Author(s):  
Jian-Kuan Li ◽  
Rui Ge ◽  
Li Tang ◽  
Qing-Shan Li
Keyword(s):  
Hydrogen Peroxide ◽  
Cardiovascular Diseases ◽  
Chinese Herb ◽  
Endothelial Injury ◽  
Potential Candidate ◽  
Protective Effects ◽  
Vsmc Proliferation ◽  
Ea.Hy926 Cells ◽  
Induced Apoptosis ◽  
Human Endothelium

Vascular endothelium plays an important role in the physiological homeostasis of blood vessels. Endothelial injury is considered to be implicated in the pathogenesis of many cardiovascular diseases, including atherosclerosis. Farrerol, a flavonoid considered to be the major bioactive component in a traditional Chinese herb, “Man-shan-hong”, which is the dried leaves of Rhododendron dauricum L., displays many bioactive properties, including antibechic, antibacterial, anti-inflammatory, and the inhibition of vascular smooth muscle cell (VSMC) proliferation. In this study, the protective effects of farrerol on hydrogen peroxide (H2O2)-induced apoptosis in human endothelium-derived EA.hy926 cells were investigated. The results showed that farrerol significantly inhibited the loss of cell viability and enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in H2O2-induced EA.hy926 cells. Meanwhile, farrerol inhibited H2O2-induced elevation in the levels of intracellular malondialdehyde and reactive oxygen species, as well as cell apoptosis. Furthermore, real time RT–PCR and Western blot analysis showed that farrerol significantly decreased the expression of Bax mRNA, Bax, cleaved caspase-3, and phosph-p38 MAPK, while increasing the exporession of Bcl-2 mRNA and Bcl-2 in H2O2-induced EA.hy926 cells. These results are the first demonstration that farrerol has protective effects against H2O2-induced apoptosis in EA.hy926 cells, and suggests that farrerol is a potential candidate for the intervention of endothelial-injury-associated cardiovascular diseases.

Dietary omega-3 alpha-linolenic acid does not prevent venous thrombosis in mice

2015 ◽  
Vol 113 (01) ◽  
pp. 177-184 ◽  
Author(s):  
Simona Stivala ◽  
Gianluigi Savarese ◽  
Giovanni G. Camici ◽  
Thomas F. Lüscher ◽  
Denisa Wagner ◽  
...  
Keyword(s):  
Mouse Model ◽  
Venous Thrombosis ◽  
Linolenic Acid ◽  
Thrombus Formation ◽  
Vena Cava ◽  
Cardiovascular Death ◽  
Endothelial Injury ◽  
Protective Effects ◽  
Omega 3 ◽  
Alpha Linolenic Acid

SummaryVenous thromboembolism (VTE) is a leading cause of cardiovascular death. Omega-3 fatty acids (n-3 FA) exhibit protective effects against cardiovascular disease. Others and our group have reported that the plant-derived n-3 FA alpha-linolenic acid (ALA) displays antiinflammatory, anticoagulant and antiplatelet effects, thereby reducing atherosclerosis and arterial thrombosis in mice fed a high ALA diet. Since procoagulant factors such as tissue factor and fibrin as well as platelets and leukocytes are crucially involved in the development of VTE, we investigated possible protective effects of dietary ALA on venous thrombus formation in a mouse model of stenosis- and furthermore, in a mouse model of endothelial injury-induced venous thrombosis. Four week old C57BL/6 mice underwent four weeks of high (7.3g%) or low ALA (0.03g%) treatment before being exposed to inferior vena cava (IVC) stenosis for 48 hours or laser injury of the endothelium of the internal jugular vein (IJV). Thrombus generation frequency, thrombus size and composition (IVC stenosis group) and time to thrombus formation (endothelial injury group) were assessed. In addition, plasma glycocalicin, a marker of platelet activation, platelet P-selectin and activated integrin expression as well as plasma thrombin generation was determined, but did not reveal any significant differences between he groups. Despite its protective properties against arterial thrombus formation, dietary ALA did not protect against venous thrombosis neither in the IVC stenosis nor the endothelial injury model, further indicating that the biological processes involved in arterial and venous thrombosis are different.

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