Protective Effect of Caffeic Acid Phenethyl Ester in Rat Cerebral Ischemia/Reperfusion Damage

• Published in: Türk nöroloji dergisi Vol. 17; no. 3; pp. 131 - 136
• Main Authors: Ertuğrul Uzar, Abdullah Acar, Uğur Fırat, Osman Evliyaoğlu, Harun Alp, Adnan Tüfek, Celal Yavuz, Sinan Demirtaş, Nebahat Taşdemir
• Format: Journal Article
• Language: English; Turkish
• Published: Galenos Yayinevi 01-01-2011
• Subjects: caffeic acid phenethyl ester; ischemia/reperfusion; Oxidative stress
• ISSN: 1301-062X

OBJECTIVE: Because oxidative stress is related to cerebral ischemia/reperfusion (I/R) injury, modulation of oxygen free radical production may represent a new approach to the management of cerebral I/R. Caffeic acid phenethyl ester (CAPE) has been determined to have neuroprotective, antioxidant, anti-inflammatory, and anti-apoptotic activities. The aim of this study was to investigate whether CAPE has a protective effect on cerebral I/R damage, and to determine the possible effects of CAPE on total antioxidant/oxidant status. METHODS: A total of 30 rats were randomly divided into three groups as control group, I/R group, and I/R + CAPE. Total oxidant status (TOS), total antioxidant status (TAS) and oxidative stress index (OSI) levels and histopathological cellular structures were evaluated in cerebral tissues obtained after the experiment procedure in all groups. RESULTS: In the brain tissue, TOS and OSI levels were found to be significantly increased in the I/R group compared to the controls (p= 0.023, p= 0.001, respectively). Significantly decreased TAS levels were found in the I/R group compared to the controls (p= 0.001). CAPE treatment prevented the increase in TOS and OSI that is produced by cerebral I/R (p= 0.041, p= 0.001, respectively). TAS was found to be increased in the CAPE + I/R group compared with the I/R group (p= 0.002). In the I/R group, the brain sections showed findings of cerebral I/R damage including inflammation, vascular congestion and necrosis (for both variables, p= 0.001). These histopathological cerebral damage findings were found to be significantly reduced in the CAPE + I/R group compared to the I/R group (for both parameters, p< 0.05). CONCLUSION: In this study, it was found that oxidative stress had an important role in the pathogenesis of cerebral I/R damage, and histopathological and biochemical evaluations showed significantly decreased I/R damage following CAPE treatment in rats.