7 research outputs found

    Protective effect of cinnamon extract against cobalt-induced multiple organ damage in rats

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    BackgroundThe role of oxidative stress and inflammation in cobalt (Co) toxicity has been the focus of previous studies. Cinnamon and its main components have been reported to have protective effects in various tissues with antioxidant and anti-inflammatory effects.AimsIn this study, the protective effect of cinnamon extract (CE) against possible Co-induced heart, kidney, and liver damage in rats was investigated biochemically.MethodsEighteen albino Wistar-type male rats were categorized into three groups (n = 6 per group): control (CG), CoCL2-administered (CoCL2), and CE + CoCL2-administered (CE + Co) groups. The CE + CoCL2 group was administered CE (100 mg/kg), and the CoCL2 and CG groups were administered distilled water orally by gavage. One hour after the administration, Co (150 mg/kg) was administered orally to the CE + CoCL2 and CoCL2 groups. This procedure was repeated once daily for 7 days. Then, biochemical markers were studied in the excised heart, kidney, and liver tissues.ResultsCoCL2 increased oxidants and proinflammatory cytokines and decreased antioxidants in heart, kidney, and liver tissues. Heart, kidney, and liver tissue were affected by Co damage. CE treatment suppressed the CoCL2-induced increase in oxidants and proinflammatory cytokines and decrease in antioxidants in heart, kidney, and liver tissues. CE treatment has been shown to attenuate cardiac damage by reducing serum troponin I (TpI) and creatine kinase-MB (CK-MB), renal damage by reducing creatinine and blood urea nitrogen (BUN), and liver damage by reducing alanine aminotransferase (ALT) and aspartate aminotransferase (AST).ConclusionCo induced the production of oxidants and proinflammatory parameters and antioxidant depletion in heart, kidney, and liver tissues of rats. Our experimental results show that CE protects heart, kidney, and liver tissues against oxidative and inflammatory changes induced by CoCLl2

    The Effect of Cerebrolysin on Ischemia Reperfusion-Induced Oxidative and Inflammatory Ovarian Damage in Rats

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    Ovarian ischemia-reperfusion (I/R) injury develops due to oxidative stress and inflammation that occurs when tissue is deprived of oxygen. Ovarian UR damage also causes infertility. The aim of this study is to see the effect of ovarian UR damage on reproductive functions and to determine the protection of antioxidant and anti-inflammatory cerebrolysin in possible damage. Albino Wistar-type female rats were divided into sham operation (SG), ischemia-reperfusion (IR) and cerebrolysin+ischemia-reperfusion (CIR) groups. After I/R application with cerebrolysin, the ovaries of six animals from each group were taken and biochemical and histopathological examinations were performed. Six animals from each remaining group were left to breed. Our test results showed that cerebrolysin decreased I/R-related oxidant, proinflammatory cytokine and tissue damage and increased antioxidant levels. In addition, cerebrolysis significantly inhibited the delay of the maternity period. These findings indicate that cerebrolysin may be helpful in the treatment of I/R-related ovarian damage and infertility

    An epidemiological study to evaluate the use of vitamin K antagonists and new oral anticoagulants among non-valvular atrial fibrillation patients in Turkey- AFTER-2 study design

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    Objectives: Atrial fibrillation (AF) is one of the most common causes of preventable ischemic stroke and is related to increased cardiovascular morbidity and mortality. There is a lack of data in Turkey on the use of new oral anticoagulants (NOACs), and time in therapeutic INR range (TTR) in vitamin K antagonist users and AF management modality. In this multi-center trial, we aimed to analyze, follow and evaluate the epidemiological data in non-valvular AF patients
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