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Mediators of Inflammation
Volume 2015, Article ID 810948, 6 pages
Research Article

Value of Caffeic Acid Phenethyl Ester Pretreatment in Experimental Sepsis Model in Rats

1Department of Infectious Diseases and Clinical Bacteriology and Department of Biochemistry, Faculty of Medicine, Fatih University, Ankara, Turkey
2Department of Infectious Diseases and Clinical Bacteriology, Fatih Sultan Mehmet Training and Research Hospital, 34746 Istanbul, Turkey
3Department of Emergency Medicine, Faculty of Medicine, Yıldırım Beyazıt University, Ankara, Turkey
4Department of Biochemistry, Faculty of Medicine, Yıldırım Beyazıt University, Ankara, Turkey
5Department of Internal Medicine, Faculty of Medicine, Ankara University, Ankara, Turkey
6Department of Biochemistry, Faculty of Medicine, Namik Kemal University, Tekirdağ, Turkey
7Department of Oncology, Faculty of Medicine, Bahcesehir University, Istanbul, Turkey

Received 23 December 2014; Revised 19 March 2015; Accepted 21 March 2015

Academic Editor: Nina Ivanovska

Copyright © 2015 Ozlem Alici et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background and Aim. The aim of this study was to determine the actions of caffeic acid phenethyl ester (CAPE) on the changes of endothelin-1 (ET-1) level, tumor necrosis factor- (TNF-) alpha, and oxidative stress parameters such as superoxide dismutase (SOD) activities and malondialdehyde (MDA) levels in experimental sepsis model in rats. Materials and Methods. Twenty-four rats were randomly divided into three experimental groups: sham (group 1), sepsis (group 2), and sepsis + CAPE (group 3), n = 8 each. CAPE was administered (10 µmol/kg) intraperitoneally to group 3 before sepsis induction. Serum ET-1, serum TNF-alpha, tissue SOD activity, and tissue MDA levels were measured in all groups. Results. Pretreatment with CAPE decreased ET-1, TNF-alpha, and MDA levels in sepsis induced rats. Additionally SOD activities were higher in rats pretreated with CAPE after sepsis induction. Conclusion. Our results demonstrate that CAPE may have a beneficial effect on ET and TNF-alpha levels and oxidative stress parameters induced by sepsis in experimental rat models. Therefore treatment with CAPE can be used to avoid devastating effects of sepsis.