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左旋 3-正丁基苯酞可改善慢性脑缺血大鼠的认知功能障碍。

L-3-n-butylphthalide improves cognitive deficits in rats with chronic cerebral ischemia.

机构信息

College of Medicine, Nankai University, 94, Weijin Rd, Tianjin 300071, China.

出版信息

Neuropharmacology. 2012 Jun;62(7):2424-9. doi: 10.1016/j.neuropharm.2012.02.014. Epub 2012 Feb 22.

Abstract

3-n-Butylphthalide (NBP) has been shown to have protective effects against ischemic stroke. In the present study, we investigated effects of l-3-n-butylphthalide (l-NBP) on the learning and memory impairment induced by chronic cerebral ischemia in rats. Male Wistar rats were administered 20 mg/kg l-NBP by gavage daily for 30 days after the bilateral common carotid artery clamping (two-vessel occlusion, 2-VO). Results showed that daily treatments of 20 mg/kg l-NBP significantly attenuated spatial learning deficits in Morris water maze (MWM) task. Results of long-term potentiation (LTP) indicated that treatment with 20 mg/kg l-NBP attenuated the inhibition of LTP in rat model of 2-VO. Moreover, l-NBP reduced glial fibrillary acidic protein (GFAP)-positive astrocytes induced by chronic cerebral ischemia. The present findings demonstrate the protective effect of l-NBP on chronic cerebral ischemia-induced hippocampus injury, which supports using l-NBP for therapy of cerebral ischemia in the future.

摘要

3-正丁基苯酞(NBP)已被证明对缺血性中风具有保护作用。在本研究中,我们研究了 l-3-正丁基苯酞(l-NBP)对慢性脑缺血诱导的大鼠学习和记忆障碍的影响。雄性 Wistar 大鼠在双侧颈总动脉夹闭(双血管闭塞,2-VO)后每日灌胃给予 20 mg/kg l-NBP,共 30 天。结果表明,每日 20 mg/kg l-NBP 治疗可显著减轻 Morris 水迷宫(MWM)任务中的空间学习缺陷。长时程增强(LTP)的结果表明,20 mg/kg l-NBP 治疗可减轻 2-VO 大鼠模型中 LTP 的抑制。此外,l-NBP 减少了慢性脑缺血引起的胶质纤维酸性蛋白(GFAP)阳性星形胶质细胞。这些发现表明 l-NBP 对慢性脑缺血诱导的海马损伤具有保护作用,这支持将来使用 l-NBP 治疗脑缺血。

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