Prune melanoidins protect against oxidative stress and endothelial cell death

10.2741/e309 ◽  
2011 ◽  
Vol E3 (3) ◽  
pp. 1034-1041
Author(s):  
Gianfranco Pintus
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Endothelial Cell ◽  
Endothelial Cell Death

Effects of Levosimendan on Inflammation and Oxidative Stress Pathways in a Lipopolysaccharide-Stimulated Human Endothelial Cell Model

2019 ◽  
Vol 21 (5) ◽  
pp. 466-472 ◽  
Author(s):  
Raquel Rodríguez-González ◽  
Piero Pollesello ◽  
Aurora Baluja ◽  
Julián Álvarez
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Endothelial Cell ◽  
Molecular Mechanisms ◽  
Cell Model ◽  
Acute Decompensated Heart Failure ◽  
Umbilical Vein ◽  
Organ Protection ◽  
Endothelial Cell Death ◽  
And Oxidative Stress

Levosimendan is a myocardial Ca2+sensitizer and opener of ATP-dependent potassium channels with inotropic, vasodilating, and cardioprotective properties. It was originally developed for the treatment of acute decompensated heart failure, but its complex mechanism of action means that it could also play a role in organ protection in response to infection. Using an in vitro approach, we explored whether levosimendan administration influenced cell responses to lipopolysaccharide (LPS). Primary human umbilical vein endothelial cells were stimulated with 1 µg/ml LPS from Escherichia coli ( E. coli). Cells were treated with levosimendan at 0, 0.1, 1, or 10 µM 3 hr later. Samples were taken 24 hr after treatment to measure cell necrosis, apoptosis, pro-inflammatory mediators (interleukin 6 [IL-6] and toll-like receptor 4 [TLR4]), and oxidative stress (total reactive oxygen species/reactive nitrogen species [ROS/RNS]). Levosimendan at 1 and 10 µM protected against LPS-induced endothelial cell death and reduced TLR4 expression ( p < .05). All doses reduced levels of IL-6 and ROS/RNS ( p < .05). Findings suggest that levosimendan may exert protective effects against endothelial cell death in this model via attenuation of inflammation and oxidative stress pathways. Future studies might explore the potential beneficial role of levosimendan in modulating molecular mechanisms triggered by infections.

Modification of Proteins in Endothelial Cell Death during Oxidative Stress

1997 ◽  
Vol 22 (7) ◽  
pp. 1277-1282 ◽  
Author(s):  
Henry P Ciolino ◽  
Rodney L Levine
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Endothelial Cell ◽  
Endothelial Cell Death

Acceleration of oxidative stress-induced endothelial cell death by nitric oxide synthase dysfunction accompanied with decrease in tetrahydrobiopterin content

Life Sciences ◽  
1997 ◽  
Vol 61 (7) ◽  
pp. 739-747 ◽  
Author(s):  
Masakazu Ishii ◽  
Shunichi Shimizu ◽  
Toshinori Yamamoto ◽  
Kazutaka Momose ◽  
Yukio Kuroiwa
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cell Death ◽  
Endothelial Cell ◽  
Nitric Oxide Synthase ◽  
Endothelial Cell Death ◽  
Oxide Synthase

Prune melanoidins protect against oxidative stress and endothelial cell death

10.2741/309 ◽  
2009 ◽  
Vol E3 (1) ◽  
pp. 1034 ◽  
Author(s):  
Anna Maria Posadino
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Endothelial Cell ◽  
Endothelial Cell Death

Severity of oxidative stress generates different mechanisms of endothelial cell death

2001 ◽  
Vol 306 (3) ◽  
pp. 409-416 ◽  
Author(s):  
A. Burlacu ◽  
V. Jinga ◽  
A. Gafencu ◽  
M. Simionescu
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Endothelial Cell ◽  
Endothelial Cell Death

Nuclear localization of endothelial nitric oxide synthase and nitric oxide production attenuates aphidicolin-induced endothelial cell death

Nitric Oxide ◽  
2021 ◽  
Vol 109-110 ◽  
pp. 12-19
Author(s):  
Jung-Hyun Park ◽  
Du-Hyong Cho ◽  
Yun-Jin Hwang ◽  
Young Min Choi ◽  
Jee Young Lee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Endothelial Cell ◽  
Nitric Oxide Synthase ◽  
Nuclear Localization ◽  
Endothelial Nitric Oxide Synthase ◽  
Nitric Oxide Production ◽  
Endothelial Cell Death ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Role of thromboxane in retinal microvascular degeneration in oxygen-induced retinopathy

2001 ◽  
Vol 90 (6) ◽  
pp. 2279-2288 ◽  
Author(s):  
Martin H. Beauchamp ◽  
Ana Katherine Martinez-Bermudez ◽  
Fernand Gobeil ◽  
Anne Marilise Marrache ◽  
Xin Hou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Endothelial Cell ◽  
Oxidant Stress ◽  
Microvascular Endothelial Cell ◽  
Oxygen Induced Retinopathy ◽  
Rat Pups ◽  
Endothelial Cell Death ◽  
Peroxidation Product ◽  
Synthase Inhibitor

Microvascular degeneration is an important event in oxygen-induced retinopathy (OIR), a model of retinopathy of prematurity. Because oxidant stress abundantly generates thromboxane A2(TxA2), we tested whether TxA2plays a role in retinal vasoobliteration of OIR and contributes to such vascular degeneration by direct endothelial cytotoxicity. Hyperoxia-induced retinal vasoobliteration in rat pups (80% O2exposure from postnatal days 5–14) was associated with increased TxB2generation and was significantly prevented by TxA2synthase inhibitor CGS-12970 (10 mg · kg−1· day−1) or TxA2-receptor antagonist CGS-22652 (10 mg · kg−1· day−1). TxA2mimetics U-46619 (EC5050 nM) and I-BOP (EC505 nM) caused a time- and concentration-dependent cell death of neuroretinovascular endothelial cells from rats as well as newborn pigs but not of smooth muscle and astroglial cells; other prostanoids did not cause cell death. The peroxidation product 8-iso-PGF2, which is generated in OIR, stimulated TxA2formation by endothelial cells and triggered cell death; these effects were markedly diminished by CGS-12970. TxA2-dependent neuroretinovascular endothelial cell death was mostly by necrosis and to a lesser extent by apoptosis. The data identify an important role for TxA2in vasoobliteration of OIR and unveil a so far unknown function for TxA2in directly triggering neuroretinal microvascular endothelial cell death. These effects of TxA2might participate in other ischemic neurovascular injuries.

Homocysteine induces cerebral endothelial cell death by activating the acid sphingomyelinase ceramide pathway

2013 ◽  
Vol 45 ◽  
pp. 21-27 ◽  
Author(s):  
Jiunn-Tay Lee ◽  
Giia-Sheun Peng ◽  
Shao-Yuan Chen ◽  
Chang-Hung Hsu ◽  
Chun-Chieh Lin ◽  
...  
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Acid Sphingomyelinase ◽  
Cerebral Endothelial Cell ◽  
Endothelial Cell Death

NGP1-01, a multi-targeted polycyclic cage amine, attenuates brain endothelial cell death in iron overload conditions

2012 ◽  
Vol 1489 ◽  
pp. 133-139 ◽  
Author(s):  
J.A. Lockman ◽  
W.J. Geldenhuys ◽  
M.R. Jones-Higgins ◽  
J.D. Patrick ◽  
D.D. Allen ◽  
...  
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Iron Overload ◽  
Brain Endothelial Cell ◽  
Endothelial Cell Death
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