Effects of aspirin on oxidative and nitrosative stress in vascular endothelial cell cultures
Abstract
|
In this study, it was aimed to investigate that whether any change in activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), lipid peroksidase and nitric oxide (NO) over time, and whether any difference between the different doses by giving different doses of aspirin to endothelial cells. Endothelial cells (HUVEC) in 24 wells microplates used in this study and 25, 50, 100, 250, 500, 750, 1000 and 1500 μM aspirin to 2 of 4 wells at each row were given, the other 2 wells were included as controls. Accordingly, while CAT, SOD, GSH-Px levels and lipid peroxidation were being measured, NO release from cell media was observed. The significant differences were not found between the baseline (0 hour) CAT, SOD, GSH-Px and lipid peroxidase levels measured from lisates that obtained from the cells that different drug doses given and controls (p>0.05). Also, CAT, SOD, GSH-Px and lipid peroxidase levels at 24 (p>0.05), 48 and 72 hours did not show any difference among different drug doses and control (p>0.05). In the control group significant differences were found between CAT, SOD and GSH-Px levels measured at 0, 24, 48, 72 hours (p<0.05, p<0.05 and p<0.05 respectively) but lipid peroxidase activity and NO levels showed no difference. Increase in antioxidant enzyme activity in the cells that aspirin was not given, caused by raised free radical formation due to increase in number of cells by time was observed. Aspirin prevented the increase in reactive enzyme activity which increases by time. These results suggest that nontoxic doses of aspirin might protect the cells. |
Keywords
References
- Antiplatelet Trialists Collaboration, Collaborative overview of randomised trials of antiplatelet therapy I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients, 1994. 308, 81-106.
- Bulckaen, H., Prévost, G., Boulanger, E., Robitaille, G., Roquet, V., Gaxatte, C., Garçon, G., Corman, B., Gosset, P., Shirali, P., Creusy, C., Puisieux, F., 2008. Low-dose aspirin prevents age-related endothelial dysfunction in a mouse model of physiological aging. Am. J. Physiol. Heart Circ. Physiol. 294, 1562-1570.
- Büssemaker, E., Pistrosch, F., Förster, S., Herbrig, K., Gross, P., Passauer, J., Brandes, R.P. 2007. Rho kinase contributes to basal vascular tone in humans: Role of endothelium-derived nitric oxide. Am. J. Physiol. Heart Circ. Physiol. 293, 541-547.
- Calver, A., Collier, J., Vallance, P., 1993. Nitric oxide and cardiovascular control. Exp. Physiol. 78, 303-326.
- Channon, K.M., Guzik, T.J., 2002. Mechanisms of superoxide production in human blood vessels: Relationship to endothelial dysfunction, clinical and genetic risk factors. Physiol. Pharmacol. 53, 515-524.
- Grosser, N., Schröder, H., 2003. Aspirin protects endothelial cells from oxidant damage via the nitric oxide-cGMP pathway. Arterioscler Thromb. Vasc. Biol. 23, 1345-1351.
- Hess, M.L., Krause, S., Kontos. H.A., 1983. Mediation of sarcoplasmic reticulum disruption in the ischemic myocardium: Proposed mechanism by the interaction of hydrogen ions and oxygen free radicals. Adv. Exp. Med. Biol. 161, 377-389.
- Hink, U., Li. H., Mollnau, H., Oelze, M., Matheis, E., Hartmann, M., Skatchkov, M., Thaiss, F., Stahl, R.A., Warnholtz, A., Meinertz, T., Griendling, K., Harrison, D.G., Forstermann, U., Munzel, T., 2001. Mechanisms underlying endothelial dysfunction in diabetes mellitus. Circ. Res. 88, 14-22.
Details
Primary Language
English
Subjects
-
Journal Section
Research Article
Authors
Emine Diraman
This is me
Yeliz Yilmaz Miroglu
This is me
Sabri Demircan
This is me
Zafer Yazici
This is me
Ahmet Yilmaz Coban
This is me
Tuba Yildirim
This is me
Ayhan Bilir
This is me
Publication Date
January 6, 2017
Submission Date
January 4, 2017
Acceptance Date
May 11, 2016
Published in Issue
Year 2016 Volume: 33 Number: 3
