Neuroprotective effects of iv tea polyphenol on cerebral ischemia reperfusion injury in animal models
Weiping Li
Abstract
Weiping Li
Abstract
Objective ] To investigate the neuroprotective effects of tea polyphenol(TP) administered intravenously on cerebral ischemia reperfusion injury in rats and mice. [Methods] (a) Complete cerebral ischemia model was made by decapitation of mice followed by recording the gasping time. (b) The mouse ischemia-reperfusion model was made by using repeated bilateral ligation and reperfusion of common carotid arteries. The SOD activities and histological neuronal changes were measured. (c) The rat model of focal cerebral ischemia was established by occluding middle cerebral artery with nylon thread. The thread was withdrawed allowing reperfusion for 24 hours after 2-hour ischemia. The neurological deficit and survival time within 24 hours were observed. [Results] (a) TP100 mg·kg -1 markedly prolonged the gasping time of mice after decapitation (0.01 P 0.05) compared with NS control. (b) TP 75 mg·kg -1 、150 mg·kg -1 could improve the histological neuronal changes and increase SOD activities in brain compared with the NS control( P 0.01). (c) TP 50 mg·kg -1 、100 mg·kg -1 significantly alleviated neurological deficit, decreased neurological deficit score ( P 0.01), and prolonged survival time within 24 hours ( P 0.01; P 0.001).after ischemia-reperfusion injury in rats compared with NS control. [Conclusion] TP administered intravenously has significant neuroprotective effects on cerebral ischemia reperfusion injury in rats and mice.
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Objective ] To investigate the neuroprotective effects of tea polyphenol(TP) administered intravenously on cerebral ischemia reperfusion injury in rats and mice. [Methods] (a) Complete cerebral ischemia model was made by decapitation of mice followed by recording the gasping time. (b) The mouse ischemia-reperfusion model was made by using repeated bilateral ligation and reperfusion of common carotid arteries. The SOD activities and histological neuronal changes were measured. (c) The rat model of focal cerebral ischemia was established by occluding middle cerebral artery with nylon thread. The thread was withdrawed allowing reperfusion for 24 hours after 2-hour ischemia. The neurological deficit and survival time within 24 hours were observed. [Results] (a) TP100 mg·kg -1 markedly prolonged the gasping time of mice after decapitation (0.01 P 0.05) compared with NS control. (b) TP 75 mg·kg -1 、150 mg·kg -1 could improve the histological neuronal changes and increase SOD activities in brain compared with the NS control( P 0.01). (c) TP 50 mg·kg -1 、100 mg·kg -1 significantly alleviated neurological deficit, decreased neurological deficit score ( P 0.01), and prolonged survival time within 24 hours ( P 0.01; P 0.001).after ischemia-reperfusion injury in rats compared with NS control. [Conclusion] TP administered intravenously has significant neuroprotective effects on cerebral ischemia reperfusion injury in rats and mice.
Key concepts: Neuroprotection, Ischemia, Medicine, Anesthesia, Neurological deficit, Reperfusion injury, Pharmacology, Internal medicine