Overexpression of Toll-Like Receptors 2, 3, 4, and 8 Is Correlated to the Vascular Atherosclerotic Process in the Hyperlipidemic Rabbit Model: The Effect of Statin Treatment

2017 ◽  
Vol 54 (3) ◽  
pp. 156-169 ◽  
Author(s):  
Alkistis Kapelouzou ◽  
Stavros Giaglis ◽  
Michalis Peroulis ◽  
Michalis Katsimpoulas ◽  
Petros Moustardas ◽  
...  
2000 ◽  
Vol 28 (02) ◽  
pp. 239-249 ◽  
Author(s):  
Mei Zhou ◽  
Yuan Chen ◽  
Qian Quyang ◽  
Shang-Xi Liu ◽  
Zhan-Jun Pang

Recent evidence has emerged that macrophage glutathione (GSH) content and selenium dependent glutathione peroxidase (SeGSHPx) activity are inversely related to cell-mediated oxidation of LDL, and intervention means to enhance the macrophage GSH-SeGSHPx status may contribute to attenuation of the atherosclerotic process. Our previous works showed that protein bound polysaccharide (PSK) injected intraperitoneally could enhance SeGSHPx activity and mRNA content of mouse macrophages. The aim of the present study is to demonstrate whether PSK can reduce the oxidative injury to the established atherosclerotic rabbits. Using the established atherosclerotic rabbit model, we studied the effect of PSK on oxidatively modified LDL (Ox-LDL), lipoperoxide (LPO) cholesterol contents and SeGSHPx activities of plasma and tissues (aorta, heart and liver) in the established atherosclerotic rabbits. As compared with the control group, Ox-LDL, LPO and cholesterol contents were much lover; SeGSHPx activities and SeGSHPx/LPO ratios were much higher in plasma and tissues (aorta, heart and liver); and the lesion area of aortae was reduced in the PSK group. Through the increment of SeGSHPx activity in macrophages and aortae, PSK enhances their antioxidation potentiality and improves the antioxidant/prooxidant imbalance in them, and thus decreases Ox-LDL, LPO and cholesterol contents of plasma and tissues, and regresses lesion area of aortae in the established atherosclerotic rabbits.


2008 ◽  
Vol 8 (4) ◽  
pp. 195-206 ◽  
Author(s):  
Adriana J. LaGier ◽  
Nick D. Manzo ◽  
Alex P. Carll ◽  
Richard H. Jaskot ◽  
Ralph Slade ◽  
...  

Author(s):  
Konstantinos S. Mylonas ◽  
Alkistis Kapelouzou ◽  
Michael Spartalis ◽  
Michael Mastrogeorgiou ◽  
Eletherios Spartalis ◽  
...  

2007 ◽  
Vol 191 (1) ◽  
pp. 82-89 ◽  
Author(s):  
Henning Steen ◽  
Antonina Kolmakova ◽  
Matthias Stuber ◽  
E Rene Rodriguez ◽  
Fabao Gao ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Guangyin Zhang ◽  
Ming Li ◽  
Yinzhi Xu ◽  
Li Peng ◽  
Cui Yang ◽  
...  

We show that hypercholesterolemia contributes to oxidative stress injury progression in brain and simvastatin counteracts the cholesterol-induced peroxidation injury in rabbit hippocampus, and we demonstrate for the first time that the simvastatin is a critical role in brain protection and identify HO-1 and other related antioxidant enzymes as molecular target for active redox compounds. Second, our experiments have pointed out an association between statin treatment and a decrease in the risk of having peroxidation damage of brain. The balance effects of simvastatin to ROS and antioxidants enzymes network are most probably due to improved SOD functional activity, increase in GSH-Px, increase in HO-1 expression, and decrease of MDA generation.


2001 ◽  
Vol 120 (5) ◽  
pp. A182-A183
Author(s):  
M HAUSMANN ◽  
S MESTERMANN ◽  
T SPOETTI ◽  
J SCHOELMERICH ◽  
T ANDUS ◽  
...  

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