AT1 Receptor Blocker Candesartan-induced Attenuation of Brain Injury of Rats Subjected to Chronic Cerebral Hypoperfusion |
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Authors: | Veysel Haktan Ozacmak Hale Sayan Alpay Cetin Aysenur Akyıldız-Igdem |
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Institution: | (1) Department of Physiology, School of Medicine, Zonguldak Karaelmas University, Kozlu, Zonguldak, 67600, Turkey;(2) Department of Pathology, Taksim Training and Research Hospital, Istanbul, Turkey |
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Abstract: | One of common pathophysiological states associated with central nervous system is chronic cerebral hypoperfusion (CH) that
frequently occurs in conditions such as vascular dementia and Alzheimer’s disease. Long term blockage of angiotensin II type
1 (AT1) receptor provides protection from ischemia induced injury of brain as well as reduction of cerebrovascular inflammation.
Examining effect of the blockage on reduced glutathione (GSH), ascorbic acid (AA), and lipid peroxidation were of purpose
in the present study. Modeling CH, rats were subjected to permanent occlusion of common carotid arteries bilaterally. AT1 receptor antagonist, candesartan, was given daily for 14 days after surgery. CH caused a significant increase in lipid peroxidation
and decrease in GSH content of cerebral hippocampal tissue with no change in AA level. Candesartan (0.5 mg/kg, oral) not only
reduced lipid peroxidation but also restored GSH significantly besides elevating AA and improving histopathological alterations.
In conclusion, long term AT1 receptor blockage may be considered as novel therapeutic approach for protection from damage associated with CH. Underlying
mechanism(s) may in part be related to suppressing oxidative stress and preserving brain antioxidant capacity. |
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Keywords: | Ascorbic acid AT1 receptor blockage Chronic cerebral hypoperfusion Glutathione Oxidative stress |
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