Danggui-Shaoyao-San ameliorates cognition deficits and attenuates oxidative stress-related neuronal apoptosis in D-galactose-induced senescent mice
Danggui-Shaoyao-San ameliorates cognition deficits and attenuates oxidative stress-related neuronal apoptosis in D-galactose-induced senescent mice
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DOI：
10.1016/j.jep.2012.02.050
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发表时间：
2012-05-07
影响因子：
5.4
通讯作者：
Ma, Shiping
中科院分区：
文献类型：
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作者：
Lan, Zhou;Liu, Jiping;Ma, Shiping
民族药理学相关性：当归芍药散（DSS）是由六味药组成的著名中药配方，已用于治疗妇科疾病和神经功能障碍。本研究的目的：本研究旨在探讨当归芍药散（DSS）对D-半乳糖（D-gal）诱导的衰老小鼠认知能力和海马氧化应激相关神经元凋亡的影响，以阐明其潜在分子机制。方法：给D-gal诱导的衰老小鼠口服DSS乙醇提取物（DE）六周。采用降压式被动回避试验和Morris水迷宫试验的方法测定认知能力。还检测了超氧化物歧化酶（SOD）和一氧化氮合酶（NOS）的活性，以及羰基蛋白（CP）、谷胱甘肽（GSH）、丙二醛（MDA）和一氧化氮（NO）的水平。此外，通过免疫组织化学法检测D-gal处理小鼠海马中凋亡相关蛋白的表达，如Bcl-2、Bax和caspase-3蛋白的表达。结果：1.8、3.6和7.2 g/kg剂量的DE显着增强了认知功能，并恢复了异常的SOD和NOS活性以及CP水平。 D-gal 诱导的 MDA、GSH 和 NO。此外，DE 通过调节 Bcl-2、Bax 和 caspase-3 的表达，改善了 D-gal 处理小鼠海马的神经细胞凋亡。结论：这些结果表明，DE 通过改善氧化应激诱导的大脑神经元凋亡，对 D-gal 诱导的衰老小鼠具有神经保护作用。 (c) 2012 Elsevier Ireland Ltd. 保留所有权利。
Ethnopharmacological relevance: Danggui-Shaoyao-San (DSS), a famous traditional Chinese medicine formula consisting of six herbal medicines, has been used to treat gynecological disorders and neural dysfunctions.Aim of the study: The present study was carried out to investigate the effects of DSS on cognitive ability and oxidative stress-related neuronal apoptosis in the hippocampus of aging mice induced by D-galactose (D-gal) to elucidate the underlying molecular mechanisms.Materials and methods: Ethanol extract of DSS (DE) were orally administered to D-gal-induced senescent mice for six weeks. The cognitive ability was determined by the methods of step-down type passive avoidance test and Morris water maze test. The activities of superoxide dismutase (SOD) and nitric oxide synthase (NOS), and levels of carbonyl protein (CP), glutathione (GSH), malondialdehyde (MDA) and nitric oxide (NO) were also examined. Furthermore, the expression of apoptotic related proteins in hippocampus of D-gal-treated mice, such as Bcl-2, Bax and caspase-3 proteins, were determined by immunohistochemistry.Results: DE at the doses of 1.8, 3.6 and 7.2 g/kg significantly enhanced the cognitive performances and restored the abnormal activities of SOD and NOS and levels of CP. MDA, GSH and NO induced by D-gal. Moreover, the neural apoptosis in the hippocampus of D-gal-treated mice was improved by DE through regulating the expression of Bcl-2, Bax and caspase-3.Conclusion: These results demonstrate that DE has neuroprotective effects in D-gal-induced senescent mice by ameliorating oxidative stress induced neuronal apoptosis in the brain. (c) 2012 Elsevier Ireland Ltd. All rights reserved.