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决明子种子对小鼠短暂性全脑缺血的神经保护作用。

The neuroprotective effects of the seeds of Cassia obtusifolia on transient cerebral global ischemia in mice.

作者信息

Kim Dong Hyun, Kim Sunho, Jung Won Yong, Park Se Jin, Park Dong Hyun, Kim Jong Min, Cheong Jae Hoon, Ryu Jong Hoon

机构信息

Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, #1 Hoeki-dong, Dongdaemoon-Ku, Seoul 130-701, Republic of Korea.

出版信息

Food Chem Toxicol. 2009 Jul;47(7):1473-9. doi: 10.1016/j.fct.2009.03.028. Epub 2009 Mar 31.

Abstract

The aim of this study was to determine the mechanism underlying the neuroprotective effects of the ethanolic extract of the seeds of Cassia obtusifolia (COE) (10 or 50mg/kg/day, p.o) on transient cerebral global ischemia induced by bilateral common carotid artery occlusion (2VO) in mice. Immunohistochemical and western blot studies showed that levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the hippocampal CA1 region at 1day post-2VO were attenuated by COE (50mg/kg/day, p.o), which was administered immediately after 2VO. Furthermore, OX-42 - and glial fibrillary acidic protein (GFAP)-positive cell numbers at 4 days post-2VO were markedly attenuated by COE (50mg/kg/day, p.o) treatment for 4 days in CA1. Viable neurons detected by Nissl at 7 days post-2VO were increased by administering COE (50mg/kg/day, p.o) for 7 days. In addition, COE increased the expressions of phosphorylated cAMP response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in CA1 in naïve-control within 1 and 6h, respectively, and these expressions were also profoundly increased in 2VO-treated mice by COE at immediately post-2VO. These results suggest that the neuroprotective effects of COE are due to its anti-inflammatory effects and to its upregulation of BDNF expression and CREB phosphorylation.

摘要

本研究的目的是确定决明子种子乙醇提取物(COE,10或50mg/kg/天,口服)对小鼠双侧颈总动脉闭塞(2VO)诱导的短暂性全脑缺血具有神经保护作用的潜在机制。免疫组织化学和蛋白质印迹研究表明,在2VO后1天,COE(50mg/kg/天,口服)可使海马CA1区诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的水平降低,COE在2VO后立即给药。此外,在2VO后4天,COE(50mg/kg/天,口服)在CA1区连续处理4天可使OX-42和胶质纤维酸性蛋白(GFAP)阳性细胞数量显著减少。在2VO后7天,通过尼氏染色检测到的存活神经元数量因给予COE(50mg/kg/天,口服)7天而增加。此外,COE分别在1小时和6小时内增加了未处理对照组CA1区磷酸化环磷酸腺苷反应元件结合蛋白(CREB)和脑源性神经营养因子(BDNF)的表达,在2VO处理的小鼠中,COE在2VO后立即给药也显著增加了这些表达。这些结果表明,COE的神经保护作用归因于其抗炎作用以及BDNF表达上调和CREB磷酸化。

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