Burns 30 (2004) 121–125 The effect of CAPE on lipid peroxidation and nitric oxide levels in the plasma of rats following thermal injury Mübin Ho¸ snuter a,∗ , Ahmet Gürel b , Orhan Babucçu a , Ferah Armutcu b , Eksal Kargi a , Ahmet I¸ sikdemir a a Department of Plastic and Reconstructive Surgery, Zonguldak Karaelmas University School of Medicine, Kozlu-Zonguldak 67600, Turkey b Department of Biochemistry, Zonguldak Karaelmas University School of Medicine, Kozlu-Zonguldak 67600, Turkey Accepted 2 September 2003 Abstract Both experimental and clinical studies have shown that oxygen-derived free radicals rise in the plasma after thermal injury and participate in the pathogenesis of tissue damage. Hence, various antioxidant molecules have been used in treatment of burn injury both experimentally and clinically. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, is known to have potent antioxidant property. The purpose of the present study was to investigate the effects of CAPE on oxidative stress in plasma of burned rats. Experiment was designed in three groups of rats with 20% full-thickness burn: (a) sham burn (n = 7); (b) burn only (n = 22); (c) burn + treatment with CAPE (n = 22). Plasma levels of malondialdehyde (MDA), nitric oxide (NO) and the activities of xanthine oxidase (XO), and superoxide dismutase (SOD) were used as both bio-indicators of oxidant status and determinant of antioxidant effect of CAPE. They were assessed by biochemical methods at 1st, 3rd, 7th, and 14th post-burn days. In conclusion, CAPE was shown to possess antioxidant activity by saving SOD activity, preventing XO activity and decreasing the levels of MDA, and NO. Our study showed that CAPE may be beneficial in burn injury. © 2003 Elsevier Ltd and ISBI. All rights reserved. Keywords: Lipid peroxidation; CAPE; Thermal injury 1. Introduction Several studies have demonstrated that burn injury ini- tiates systemic inflammatory reactions by producing burn toxins, reactive oxygen species (ROS) and finally leads to peroxidation [1,2]. Underlying mechanism of this event is the deformation of cell membrane phospholipids by oxidiz- ing radicals. Cell membranes are rich sources of polyun- saturated fatty acids (PUFAs). The oxidative destruction of PUFAs is known as lipid peroxidation which causes tissue injury. An intense affiliation has been demonstrated be- tween the quantity of lipid peroxidation and the degree of burn complications such as remote organ damage and shock [3,4]. Reactive oxygen species are produced constantly in cells with normal metabolism. On the other hand, cells are able to defend themselves from destructive potential of ∗ Corresponding author. Tel.: +90-372-2610169; fax: +90-372-2610155. E-mail address: hosnuter@karaelmas.edu.tr (M. Ho¸ snuter). oxygen radicals in normal physiologic condition by way of their own antioxidant mechanisms including enzyme sys- tems, vitamins, elements, and some antioxidant molecules [5]. There is an exquisite balance between production and destruction of ROS. When this equilibrium is destroyed, ROS are produced excessively and all tissues are exposed to oxidative injury [6]. Several studies have demonstrated the effectiveness of antioxidants in scavenging free oxygen radicals. Cur- rently, therapeutic application of both enzymatic and non- enzymatic antioxidants such as: alpha-tocopherol, ascorbic acid, ceruloplasmin, desferrioxamine, allopurinol, N-ace- tylcysteine, and superoxide dismutase (SOD) have been shown to be important [7–9]. Caffeic acid phenethyl ester (CAPE) has been identified as a main active ingredient of propolis which is a honeybee hive product. It has been used in folk medicine for many years in the treatment of various ailments. Several important pharmaceutical properties have been ascribed to propolis, including anti-inflammatory, and antioxidant activities [10]. 0305-4179/$30.00 © 2003 Elsevier Ltd and ISBI. All rights reserved. doi:10.1016/j.burns.2003.09.022