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小麦醇溶蛋白对β-淀粉样蛋白诱导的细胞死亡和记忆损伤的神经保护作用。

Neuroprotective effects of Triticum aestivum L. against beta-amyloid-induced cell death and memory impairments.

机构信息

College of Oriental Medicine, Daegu Haany University, Sang-dong, Suseong-gu, Daegu 706-060, Korea.

出版信息

Phytother Res. 2010 Jan;24(1):76-84. doi: 10.1002/ptr.2871.

DOI:10.1002/ptr.2871
PMID:19441012
Abstract

beta-Amyloid (A beta) is a key component of senile plaques, neuropathological hallmarks of Alzheimer's disease (AD) and has been reported to induce cell death via oxidative stress. This study investigated the protective effects of Triticum aestivum L. (TAL) on A beta-induced apoptosis in SH-SY5Y cells and cognitive dysfunctions in Sprague-Dawley (SD) rats. Cells treated with A beta exhibited decreased viability and apoptotic features, such as DNA fragmentation, alterations in mitochondria and an increased Bax/Bcl-2 ratio, which were attenuated by TAL extract (TALE) pretreatment. To elucidate the neuroprotective mechanisms of TALE, the study examined A beta-induced oxidative stress and cellular defense. TALE pretreatment suppressed A beta-increased intracellular accumulation of reactive oxygen species (ROS) via up-regulation of glutathione, an essential endogenous antioxidant. To further verify the effect of TALE on memory impairments, A beta or scopolamine was injected in SD rats and a water maze task conducted as a spatial memory test. A beta or scopolamine treatment increased the time taken to find the platform during training trials, which was decreased by TALE pretreatment. Furthermore, one of the active components of TALE, total dietary fiber also effectively inhibited A beta-induced cytotoxicity and scopolamine-caused memory deficits. These results suggest that TALE may have preventive and/or therapeutic potential in the management of AD.

摘要

β-淀粉样蛋白(Aβ)是老年斑的关键组成部分,也是阿尔茨海默病(AD)的神经病理学标志,并已被报道通过氧化应激诱导细胞死亡。本研究调查了小麦(Triticum aestivum L.)(TAL)对 Aβ诱导的 SH-SY5Y 细胞凋亡和 Sprague-Dawley(SD)大鼠认知功能障碍的保护作用。用 Aβ处理的细胞表现出活力降低和凋亡特征,如 DNA 片段化、线粒体改变和 Bax/Bcl-2 比值增加,这些特征在 TAL 提取物(TALE)预处理后得到缓解。为了阐明 TALE 的神经保护机制,研究检查了 Aβ诱导的氧化应激和细胞防御。TALE 预处理通过上调谷胱甘肽抑制 Aβ增加的细胞内活性氧(ROS)积累,谷胱甘肽是一种必需的内源性抗氧化剂。为了进一步验证 TALE 对记忆损伤的影响,将 Aβ或东莨菪碱注射到 SD 大鼠中,并进行水迷宫任务作为空间记忆测试。Aβ或东莨菪碱处理增加了训练试验中找到平台的时间,而 TALE 预处理则减少了这一时间。此外,TALE 的一种活性成分,总膳食纤维也有效抑制了 Aβ诱导的细胞毒性和东莨菪碱引起的记忆缺陷。这些结果表明,TALE 可能在 AD 的管理中具有预防和/或治疗潜力。

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