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    The Neuroprotective Effect of Glycyrrhizic Acid on an Experimental Model of Focal Cerebral Ischemia in Rats
    (Springer/Plenum Publishers, 2015) Akman, Tarik; Guven, Mustafa; Aras, Adem Bozkurt; Ozkan, Adile; Sen, Halil Murat; Okuyucu, Ali; Kalkan, Yildiray
    Cerebral ischemia is still one of the most important topics in neurosciences. Our study aimed to investigate the neuroprotective and anti-oxidant effects of glycyrrhizic acid on focal cerebral ischemia in rats. Twenty-four rats were divided equally into three groups. A middle cerebral artery occlusion model was performed in this study where sham and glycyrrhizic acid were administered intraperitoneally following middle cerebral artery occlusion. Group I was evaluated as control. Malondialdehyde (MDA), superoxide dismutase (SOD), and nuclear respiratory factor-1 (NRF1) levels were analyzed biochemically on the right cerebral hemisphere, while ischemic histopathological studies were completed to investigate the anti-oxidant status. Biochemical results showed that SOD and NRF1 levels were significantly increased in the glycyrrhizic acid group compared with the sham group while MDA levels were significantly decreased. On histopathological examination, cerebral edema, vacuolization, degeneration, and destruction of neurons were decreased in the glycyrrhizic acid group compared with the sham group. Cerebral ischemia was attenuated by glycyrrhizic acid administration. These observations indicate that glycyrrhizic acid may have potential as a therapeutic agent in cerebral ischemia by preventing oxidative stress.
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    Öğe
    The protective effect of syringic acid on ischemia injury in rat brain
    (Tubitak Scientific & Technological Research Council Turkey, 2015) Guven, Mustafa; Aras, Adem Bozkurt; Topaloglu, Naci; Ozkan, Adile; Sen, Halil Murat; Kalkan, Yildiray; Okuyucu, Ali
    Background/aim: Brain ischemia and treatment are important topics in neurological science. Free oxygen radicals and inflammation formed after ischemia are accepted as the most significant causes of damage. Currently there are studies on many chemopreventive agents to prevent cerebral ischemia damage. Our aim is to research the preventive effect of the active ingredient in syringic acid, previously unstudied, on oxidative damage in cerebral ischemia. Materials and methods: The rats were randomly divided into 4 groups: control group (no medication or surgical procedure), sham group (artery occlusion), artery occlusion + syringic acid group sacrificed at 6 h, and artery occlusion + syringic acid group sacrificed at 24 h. Obtained brain tissue from the right hemisphere was investigated histopathologically and for tissue biochemistry. Results: Superoxide dismutase and nuclear respiratory factor 1 values decreased after ischemia and they increased after syringic acid treatment, while increased malondialdehyde levels after ischemia were reduced after treatment. Caspase-3 and caspase-9 values increased after ischemia and decreased after treatment; this reduction was more pronounced at 24 h. Conclusion: Our study revealed that syringic acid treatment in cerebral ischemia reduced oxidative stress and neuronal degeneration. In the light of the biochemical and histopathologic results of the present study, we think that syringic acid treatment may be an alternative treatment method.