Comparison neuroprotective effects of ellagic acid and aliskren after cerebral ischemia

Comparison neuroprotective effects of ellagic acid and aliskren after cerebral ischemia Kamuran Aydın, Dicle University Faculty of Medicine, Department of Neurosurgery, Diyarbakır / TURKEY Introduction and aim: Stroke, which is an important cause of morbidity and mortality, can be classified an ischemic and hemorrhagic in general. Cerebral ischemia the failure to main the oxygenation required for cerebral tissues due to the decrease in cerebral blood flow. In thrombosis, there is an obsructive process in the structures that provide blood flow to some regions of the brain. Atherosclerosis, vasculitis and arterial dissections carry a risk of thrombosis. In contrast, embolism is caused by a clot that originates from anoher part of body and is most commonly caused by the heart. Neuroprotection studies originated from pathological studies of ischemic brain injury. Sudden low levels of oxygen and glucose in neural tissues initiate a series of pathological cascades leading to neuronal loss. If one of these steps can be prevented, it is thought that some brain tissue can be preserved. Neuroprotective agents designed to block this cascade have been investigated in animal models in recent years. Ellagic acid is an natural antioxidant. In different studies, ıt has been shown that ellagic acid may have antioxidant, antiviral, antimicrobial effects, protective effects on the cardiovascular system and protective effects in neurodegenerative diseases. Aliskiren is the first orally active, nonpeptide renin inhibitör and is accepted in the treatment of hypertension and can be used alone or in combination with other antihypertensive drugs. We investigated the neuroprotective effects of these substances in rats with ischemia induced. Materials and methods: In our study, randomly selected 18 Sprague-Dawley type female and male rats were used. After 4 hours of fasting, rats were anesthetized with 80 mg/kg ketamine and 10 mg/kg xylazine. The catheter vas advanced through the ight internal carotid and placed so as to occlude the proximal middle cerebral artery and left for 2 hours. Then it vas withdrawn an recanalization was achived. Rats were divided into three groups. After ischemia, the first group was the control group and no treatment was given, the second group was given a single döşe of ellegic acid at a dose 30 mg/kg for a week, and the third group was given a dose of 2,5 mg/kg aliskiren once a day for a week. One week later, the rats were sacrificed and their brain tissues were removed under sterile conditions. Extracted brain tissues were stained with Hematoxylin-Eosin and Toluidine Blue. Pycnosis in neural cells, pycnosis in glial cells, neuron cell degeneration, glial cell degeneration and vascular degeneration were evaluated by the same histopathologist. Results: Both ellagic acid and aliskiren showed a decrease pycnosis in neural cells, pycnosis in glial cells, neuron degeneration, glial degeneration and vascular degeneration compared to the control group. Ellagic acid provided a statistically significant reduction in pycnosis in neural cells, pycnosis in glial cells and neuron cell degeneration compared to aliskirene. On the other hand, although ellagic acid reduces glial cell degeneration and vascular degeneration more than aliskiren histologically, no statistically significant difference was found between the effects of two drugs. Conclusion: The neuroprotective effects of both ellagic acid and aliskiren were seen in ischemia, and it was concluded they could be included in treatment protocols after further experimental studies. Keywords: Rat, Ischemia, Ellagic acid, Aliskiren, Neuroprotective