2002•Unpublished venueRequires access

Protective effect of abelmischl manihot l.medic against cerebral ischemia-reperfusion injury

Zhi Chen

Open publisher page 2 citations

Abstract

AIM To study the protective effect of TFA against cerebral ischemia reperfusion injury. METHORDS The cerebral ischemia model in mice was made by means of ligating bilalateral common carotid arteries.The mice survive rate during 6 h was observed,and malondialdehyde (MDA) in the ischemic cerebral cortex was measured. Using nitrogen anoxia model in mice,the survive time was observed. Ligating bilateral common carotid arteries and descending blood pressure,the cerebral ischemia reperfusion model in rabbits was established. The brain of rabbits was initiated by ischemia for 60 min followed by 30 min of reperfusion. The electroencephalogra phy (EEG) of cerebral ischemia and reperfusion was recorded. Malondialdehyde(MDA) and lactate dehydrogenase(LDH) in the ischemic cerebral cortex were measured. RESULTS TFA(30,60,120 mg·kg -1 ) prolonged the survive time after anoxia in mice,enchanced the survive rate after cerebral ischemia and inhibited the increasing of MDA contents in the cerebral cortex in mice.TFA(12,24,48 mg·kg -1 ) inhibitid the changes of EEG,MDA and LDH induced by cerebral ischemia reperfusion in rabbits. CONCLUSION TFA has protective effects on cerebral ischemia reperfusion injury,the mechanism may relate to attenuating free radical and lipid peroxidation.

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AIM To study the protective effect of TFA against cerebral ischemia reperfusion injury. METHORDS The cerebral ischemia model in mice was made by means of ligating bilalateral common carotid arteries.The mice survive rate during 6 h was observed,and malondialdehyde (MDA) in the ischemic cerebral cortex was measured. Using nitrogen anoxia model in mice,the survive time was observed. Ligating bilateral common carotid arteries and descending blood pressure,the cerebral ischemia reperfusion model in rabbits was established. The brain of rabbits was initiated by ischemia for 60 min followed by 30 min of reperfusion. The electroencephalogra phy (EEG) of cerebral ischemia and reperfusion was recorded. Malondialdehyde(MDA) and lactate dehydrogenase(LDH) in the ischemic cerebral cortex were measured. RESULTS TFA(30,60,120 mg·kg -1 ) prolonged the survive time after anoxia in mice,enchanced the survive rate after cerebral ischemia and inhibited the increasing of MDA contents in the cerebral cortex in mice.TFA(12,24,48 mg·kg -1 ) inhibitid the changes of EEG,MDA and LDH induced by cerebral ischemia reperfusion in rabbits. CONCLUSION TFA has protective effects on cerebral ischemia reperfusion injury,the mechanism may relate to attenuating free radical and lipid peroxidation.

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Available abstract

AIM To study the protective effect of TFA against cerebral ischemia reperfusion injury. METHORDS The cerebral ischemia model in mice was made by means of ligating bilalateral common carotid arteries.The mice survive rate during 6 h was observed,and malondialdehyde (MDA) in the ischemic cerebral cortex was measured. Using nitrogen anoxia model in mice,the survive time was observed. Ligating bilateral common carotid arteries and descending blood pressure,the cerebral ischemia reperfusion model in rabbits was established. The brain of rabbits was initiated by ischemia for 60 min followed by 30 min of reperfusion. The electroencephalogra phy (EEG) of cerebral ischemia and reperfusion was recorded. Malondialdehyde(MDA) and lactate dehydrogenase(LDH) in the ischemic cerebral cortex were measured. RESULTS TFA(30,60,120 mg·kg -1 ) prolonged the survive time after anoxia in mice,enchanced the survive rate after cerebral ischemia and inhibited the increasing of MDA contents in the cerebral cortex in mice.TFA(12,24,48 mg·kg -1 ) inhibitid the changes of EEG,MDA and LDH induced by cerebral ischemia reperfusion in rabbits. CONCLUSION TFA has protective effects on cerebral ischemia reperfusion injury,the mechanism may relate to attenuating free radical and lipid peroxidation.

Key concepts: Malondialdehyde, Ischemia, Anesthesia, Medicine, Cerebral cortex, Reperfusion injury, Lactate dehydrogenase, Lipid peroxidation

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