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    Protective effect of caffeic acid phenethyl ester in rat cerebral ischemia/reperfusion damage
    (Turkish Neurosurgical Society, 2011) Uzar E.; Acar A.; Firat U.; Evliyaoğlu O.; Alp H.; Tüfek A.; Yavuz C.
    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.
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    The protective effect of dexmedetomidine on bupivacaineinduced sciatic nerve inflammation is mediated by mast cells
    (2013) Tüfek A.; Kaya S.; Tokgöz O.; Firat U.; Evliyaoğlu O.; Çelik F.; Karaman H.
    Purpose: This study was designed to assess the correlation between the neuroprotective effect of dexmedetomidine and oxidative stress, neural inflammation and mast cell stability in rats with bupivacaine-induced sciatic nerve toxicity. Methods: Forty adult Wistar Albino rats, eight rats per group, were used. Saline (0.3 ml of 0.9%), dexmedetomidine (20 ?g/kg), 0.5% bupivacaine or 0.5% bupivacaine+dexmedetomidine (20 ?g/kg) was injected into the sciatic nerve. A control group of rats received no injection. Fourteen days after injection, the sciatic nerves were harvested and total oxidant status, total anti-oxidant status, paraoxonase-1, galectin-3 and matrix metalloproteinase 2 and 9 levels were measured in the sciatic nerves. In addition, the presence and status of inflammation, edema, and mast cells were evaluated histopathologically. Results: The combination of dexmedetomidine and bupivacaine alleviated oxidative stress. In addition, it decreased matrix metalloproteinase 9 and galectin-3 levels and increased matrix metalloproteinase 2 levels. Moreover, it stabilized recruited mast cells at the injury site; however, it did not significantly decrease inflammation or edema. Conclusion: Dexmedetomidine may ameliorate bupivacaine-induced neurotoxicity by modulating mast cell degranulation. The neuroprotective effect of dexmedetomidine may make it a suitable adjuvant agent to local anesthetics in peripheral nerve blocks.
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    Öğe
    The relationship between coenzyme Q10 and severity of coronary artery disease
    (2013) Büyükkaya E.; Evliyaoğlu O.; Islamoğlu Y.; Cil H.; Karakaş M.F.; Akçay A.B.; Bilen P.
    Aim To evaluate the relationship between the levels of plasma coenzyme Q10 (CoQ10), a known antioxidant, and severity of the coronary atherosclerosis (AS) measured by Gensini score. Methods Patients with coronary artery disease (CAD) were enrolled to the study between 2010 and 2011 in cardiology outpatient clinics. They were admitted for diagnostic coronary angiography or angioplasty for typical indications. The Gensini scoring system was used to calculate CAD severity. Serum CoQ10, total cholesterol (TC), HDL cholesterol, LDL cholesterol, and triglyceride levels were assessed. Results One hundred thirteen subjects (83 CAD, 30 controls) were included. The patients with CAD were separated into three groups according to Gensini score. The serum levels of CoQ10, CoQ10/ TC, CoQ10/LDL-C, CoQ10/TG rates in the subjects of mild and severe AS groups were significantly lower than the control group (p<0.016 for all control vs. AS group comparisons). There were no significant differences in serum levels of CoQ10 and CoQ10/ TC, CoQ10/LDL-C, CoQ10/TG rates between the mild and severe AS groups. Conclusion This study revealed that although the serum CoQ10 levels were lower in stable CAD, there was no relationship between the severity of CAD and serum CoQ10 levels in patients with stable angina pectoris.