Antioxidant Activity-Mediated Neuroprotective Effects of an Antagonist of AT1 Receptors, Candesartan, Against Cerebral Ischemia and Edema in Rats
We examined the effects of post-ischemic blockade of angiotensinAT1 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 ische...
Збережено в:
Дата: | 2013 |
---|---|
Автори: | , , |
Формат: | Стаття |
Мова: | English |
Опубліковано: |
Інститут фізіології ім. О.О. Богомольця НАН України
2013
|
Назва видання: | Нейрофизиология |
Онлайн доступ: | http://dspace.nbuv.gov.ua/handle/123456789/148233 |
Теги: |
Додати тег
Немає тегів, Будьте першим, хто поставить тег для цього запису!
|
Назва журналу: | Digital Library of Periodicals of National Academy of Sciences of Ukraine |
Цитувати: | Antioxidant Activity-Mediated Neuroprotective Effects of an Antagonist of AT1 Receptors, Candesartan, Against Cerebral Ischemia and Edema in Rats / H. Panahpour, Sh. Bohlooli, S.E. Motavallibashi // Нейрофизиология. — 2013. — Т. 45, № 5. — С. 469-475. — Бібліогр.: 37 назв. — англ. |
Репозитарії
Digital Library of Periodicals of National Academy of Sciences of UkraineРезюме: | We examined the effects of post-ischemic blockade of angiotensinAT1 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. |
---|