اثرات کندسارتان، آنتاگونیست گیرنده های نوع یک آنژیوتانسین دو بر ایسکمی مغزی و ادم مغزی از طریق فعالیت آنتی اکسیدانی واسطه گری می شود

عنوان انگليسی

Antioxidant Activity-Mediated Neuroprotective Effects of an Antagonist of AT1 Receptors, Candesartan, against Cerebral Ischemia and Edema in Rats

خلاصه انگلیسی

We examined the effects of post-ischemic blockade of angiotensin AT1 receptors by candesartan on cerebral infarction and formation of edema. Male Sprague–Dawley rats were divided into three groups, sham, control ischemic, and candesartan-treated (0.3 mg/kg) ischemic. Transient focal cerebral ischemia was induced by 90-min-long occlusion of the left middle cerebral artery followed by 24-h-long reperfusion. Neurological deficit score was evaluated at the end of the reperfusion period. Thereafter, the animals were randomly selected and used for three projects: (i) Measurement of the infarct volumes, (ii) investigation of ischemic brain edema formation using a wet/dry method, and (iii) assessment of the malondialdehyde (MDA) and reduced glutathione (GSH) concentrations using a HPLC technique. Induction of cerebral ischemia in the control group produced considerable infarctions in the cortex and striatum in conjunction with severely impaired motor functions. Candesartan treatment significantly reduced the infarct volumes and improved the above functions. The water content in the left (lesioned) hemisphere was considerably elevated in the control ischemic group. Candesartan treatment significantly lowered the water content in the ischemic lesioned hemisphere, retained tissue GSH level, and led to a lower MDA production. AT1 receptor blockade by candesartan treatment can noticeably decrease ischemic brain injury and attenuate edema formation, likely via increasing the antioxidant activity.

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