Abstract TP136: Cilostazol Inhibits Inflammation and Endothelial Cell Damage in Patients with Severe Carotid Disease

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Masako Yamazaki ◽  
Yoshikazu Okada ◽  
Akitsugu Kawashima ◽  
Koji Yamaguchi ◽  
Taku Yoneyama ◽  
...  

Background: Cilostazol is an antiplatelet agent, which is known also to have protective effects on endothelial cell. We studied effects of cilostazol on markers of inflammation and endothelial cell damage in patients with severe carotid disease, who underwent carotid endoarterectomy (CEA). Methods: We measured high sensitivity CRP (hsCRP), soluble vascular cellular adhesion molecule (VCAM)-1, soluble E-selectin, soluble intercellular adhesion molecule-1 and von Willebrand Factor antigen (vWF) in 45 patients who underwent CEA (38 males and 7 females, mean age was 69 years). Venous blood was taken from each patient before (Pre) and 3 days (Day3), 10 days (Day10), 4 weeks and 1 year (Post) after CEA. Each marker was compared between patients who were treated with aspirin alone (aspirin group, 18 cases) and those treated with cilostazol alone or cilostazol plus aspirin (cilostazol group, 17 cases). Results: The levels of hsCRP, VCAM-1, E-selectin and vWF at Day3 and the levels of hsCRP and VCAM-1 on Day10 were significantly higher than those at PreCEA. The alterations of those markers were not significantly different between the aspirin and cilotazol groups. The levels of hsCRP in the cilostazol group were significantly lower than those in aspirin group at both PreCEA and PostCEA. The levels of VCAM-1 at PreCEA in the cilostazol group were significantly lower than those in the aspirin group. Conclusions: The results suggested that cilostazol inhibits inflammation and endothelial cell damage in patients with severe carotid disease, although its protective effects did not reduce the endothelial cell damage induced by CEA when compared with aspirin.

2012 ◽  
Vol 139 (2) ◽  
pp. 388-394 ◽  
Author(s):  
Zi-lin Li ◽  
Jin-cheng Liu ◽  
Jing Hu ◽  
Xiao-qiang Li ◽  
Si-wang Wang ◽  
...  

TH Open ◽  
2017 ◽  
Vol 01 (01) ◽  
pp. e3-e10 ◽  
Author(s):  
Toshiaki Iba ◽  
Tetsuya Sasaki ◽  
Kazutoshi Ohshima ◽  
Koichi Sato ◽  
Isao Nagaoka ◽  
...  

AbstractAntithrombin is a promising option for the treatment of sepsis, and vascular endothelium is an important target for this fatal condition. Here, we aimed to evaluate the protective effects of different glycoforms of antithrombin on histone-induced endothelial cell damage and explore the responsible mechanisms in an experimental model in vitro. Endothelial cells were treated in vitro using histone H4 to induce cellular damage. Various doses of either α- or β-antithrombin were used as treatment interventions, and both cell viability and the levels of lactate dehydrogenase (LDH) in the medium were assessed. Endothelial cell damage was also assessed using microscopic examination and immunofluorescent staining with anti-syndecan-4 and anti-antithrombin antibodies. As a result, both glycoforms of antithrombin significantly improved cell viability when administered at a physiological dose (150 μg/mL). Cellular injury as evaluated using the LDH level was significantly suppressed by β-antithrombin at a supranormal dose (600 μg/mL). Microscopic observation suggested that β-antithrombin suppressed the endothelial cell damage more efficiently than α-antithrombin. β-Antithrombin suppressed the intensity of syndecan-4 staining which became evident after treatment with histone H4, more prominently than α-antithrombin. The distribution of antithrombin was identical to that of syndecan-4. In conclusion, both α- and β-antithrombin can protect vascular endothelial cells from histone H4-induced damage, although the effect was stronger for β-antithrombin. The responsible mechanisms might involve the binding of antithrombin to the glycocalyx on the endothelial surface. These results provide a theoretical basis for the application of antithrombin to the prevention and treatment of sepsis-related endothelial damage.


2005 ◽  
Vol 19 (3) ◽  
pp. 398-406 ◽  
Author(s):  
Harold W. Davis ◽  
Elizabeth VandenBerg ◽  
Maria D. Reid ◽  
Prabir Roy-Chaudhury ◽  
John D. Edwards

2014 ◽  
Vol 912-914 ◽  
pp. 1965-1968
Author(s):  
Wen He Zhu ◽  
Wei Zhang ◽  
Ying Xin Qin ◽  
Nan Shen ◽  
Li Jing Zhao ◽  
...  

Abstract: Objective: To investigate whether the extract of Juglans mandshurica maxim could inhibits the apoptosis induced by endogenous H2O2 on Endothelial Cell (EVC-304)in vitro. METHODS: Cultured EVC-304 cells were incubated with 10mUGOX or with 10mUGOX and different concentrations (25μg/ mL, 50μg/ mL, 100μg/ mL) of the extract of Juglans mandshurica maxim for 24h.The proliferation of EVC-304cells was detected by methyl thiazolyl tetrazolium (MTT) assay. The early apoptotic percent was measured by flow cytometry (FCM). RESULTS: MTT results showed that the inhibition proliferation of EVC-304 cells induced by endogenous H2O2 could be inhibited by the extract of Juglans mandshurica maxim in a dose -dependent manner. FCM assay indicated that, after treatment on EVC-304 cells with endogenous H2O2, the early apoptotic percent was increased, but the apoptosis rate was decreased significantly when the extract of Juglans mandshurica maxim added. CONCLUSION: the extract of Juglans mandshurica maxim protected significantly the cell damage and cell apoptosis induced by endogenous H2O2.


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