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鞣花酸通过调节 Bcl-2/Bax 表达的比值来防止脑缺血性中风引起的神经元损伤。

Ellagic acid protects against neuron damage in ischemic stroke through regulating the ratio of Bcl-2/Bax expression.

机构信息

a Key Lab of Ministry of Education, National Research Center on Minority Medicine and Translational Neuroscience, Minzu University of China, Beijing 100081, People's Republic of China.

b Experimental Research Center, China Academy of traditional Chinese Medicine, Beijing, 100700, People's Republic of China.

出版信息

Appl Physiol Nutr Metab. 2017 Aug;42(8):855-860. doi: 10.1139/apnm-2016-0651. Epub 2017 Apr 7.

DOI:10.1139/apnm-2016-0651
PMID:28388366
Abstract

An oxygen-glucose deprivation and reoxygenation model in primary cultured rat cortical neurons was developed for this study to investigate the effects of ellagic acid (EA), a low-molecular-weight polyphenol, on neuron cells and their function, and to evaluate whether EA can be safely utilized by humans as a functional food or therapeutic agent. Administration of EA significantly decreased the volume of cerebrum infarction and the neurological deficit scores of the rats; EA treatment also increased the number of Bcl-2-positive cells and the ratio of Bcl-2-positive to Bax-positive neurons in the semidarkness zone near the brain ischemic focus in the photothrombotic cerebral ischemia model. Treatment of EA resulted in increased neuron viability, cell nuclear integrity, and the ratio of Bcl-2/Bax expression in the primary cultured neuron model; EA treatment also lead to a decrease in the number of apoptotic cells. Our results therefore suggest a specific mechanism for the beneficial effects of EA, providing new insights into how it provides neuroprotection. To the best of our knowledge, these results represent new insights on the mechanisms of the brain cell protective activity of EA. Thus, EA may be used in functional foods or medicines to help treat nerve dysfunction, neurodegenerative disease, and aging.

摘要

本研究建立了原代培养大鼠皮质神经元氧葡萄糖剥夺再复氧模型,以研究鞣花酸(EA)对神经元细胞及其功能的影响,并评估 EA 是否可安全地作为功能性食品或治疗剂被人类利用。EA 的给药显著降低了脑梗死体积和大鼠的神经功能缺损评分;EA 治疗还增加了光血栓性脑缺血模型中脑缺血灶附近半暗带中 Bcl-2 阳性细胞的数量和 Bcl-2 阳性/ Bax 阳性神经元的比例。EA 处理导致原代培养神经元模型中的神经元活力、核完整性以及 Bcl-2/Bax 表达的比例增加;EA 处理还导致凋亡细胞数量减少。因此,我们的结果表明 EA 的有益作用的特定机制,为其提供神经保护作用的机制提供了新的见解。据我们所知,这些结果代表了对 EA 脑细胞保护活性的机制的新见解。因此,EA 可用于功能性食品或药物,以帮助治疗神经功能障碍、神经退行性疾病和衰老。

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