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亚马逊草药玛拉帕尤玛可减轻阿尔茨海默病小鼠的认知障碍和神经胶质变性。

The Amazonian herbal Marapuama attenuates cognitive impairment and neuroglial degeneration in a mouse Alzheimer model.

机构信息

Laboratório de Etnofarmacologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Sarmento Leite 500, Porto Alegre, RS, Brazil.

出版信息

Phytomedicine. 2011 Feb 15;18(4):327-33. doi: 10.1016/j.phymed.2010.07.013. Epub 2010 Aug 23.

Abstract

UNLABELLED

Alzheimer's disease (AD) is expected to affect more than 22 million people worldwide by 2025, causing devastating suffering and enormous costs to families and society. AD is a multifactorial disease, with a complex pathological mosaic. In rodents, AD-like dementia can be induced by cerebral microinjection of Aβ peptide, leading to amyloid deposits, amnesia and various features of neurodegeneration. Marapuama (Ptychopetalum olacoides) is regarded as a "brain tonic" in the Amazon region and shows a nootropic profile in rodents.

AIM OF THE STUDY

Because a specific extract (POEE) of Marapuama was shown to possess promnesic and anti-amnesic properties, the aim of this study was to verify if POEE is also effective against Aβ(1-42)-induced cognitive deficit in mice. Additionally, Aβ deposits (Congo red), GFAP immunoreactivity (immunohistochemistry), and neurodegenerative changes in the hippocampal pyramidal layer (Nissl) were examined as measures of Aβ(1-42)-induced neurodegeneration.

MATERIALS AND METHODS

CF1 mice were subjected to the experimental Alzheimer model with the Aβ(1-42) i.c.v. administration. The effects of POEE 800 mg/kg were evaluated over 14 consecutive days of treatment.

RESULTS

The data show that 14 days of oral treatment with POEE (800 mg/kg) was effective in preventing Aβ-induced cognitive impairment, without altering the levels of BDNF and with parallel reductions in Aβ deposits and astrogliosis. CA1 hippocampus loss induced by Aβ(1-42) was also diminished in POEE-treated mice.

CONCLUSION

This study offers evidence of functional and neuroprotective effects of two weeks treatment with a Ptychopetalum olacoides extract against Aβ peptide-induced neurotoxicity in mice. Given the multifactorial nature of neurodegeneration, the considerable potential for an AChE inhibitor displaying associated neuroprotective properties such as here reported warrants further clinic evaluation.

摘要

未注明

到 2025 年,预计全球将有超过 2200 万人受到阿尔茨海默病(AD)的影响,给家庭和社会带来毁灭性的痛苦和巨大的成本。AD 是一种多因素疾病,具有复杂的病理镶嵌。在啮齿动物中,Aβ肽的脑内微注射可诱导类似 AD 的痴呆,导致淀粉样沉积、健忘症和各种神经退行性变特征。马鲁帕玛(Ptychopetalum olacoides)在亚马逊地区被视为“大脑补品”,并在啮齿动物中表现出益智作用。

研究目的

由于马鲁帕玛的一种特定提取物(POEE)显示出促智和抗健忘特性,本研究旨在验证 POEE 是否也能有效对抗 Aβ(1-42)诱导的小鼠认知障碍。此外,还检查了 Aβ 沉积(刚果红)、GFAP 免疫反应性(免疫组织化学)和海马锥体层的神经退行性变化(尼氏染色),作为 Aβ(1-42)诱导的神经退行性变的衡量标准。

材料和方法

CF1 小鼠接受 Aβ(1-42)脑室内给药的实验性阿尔茨海默病模型。评价 POEE 800mg/kg 连续 14 天治疗的效果。

结果

数据显示,口服 POEE(800mg/kg)治疗 14 天可有效预防 Aβ 诱导的认知障碍,而不改变 BDNF 水平,并平行减少 Aβ 沉积和星形胶质增生。POEE 治疗小鼠的 Aβ(1-42)诱导的 CA1 海马丢失也减少。

结论

本研究提供了两星期用 Ptychopetalum olacoides 提取物治疗的功能和神经保护作用的证据,对抗 Aβ 肽诱导的小鼠神经毒性。鉴于神经退行性变的多因素性质,具有这种报道的相关神经保护特性的 AChE 抑制剂具有相当大的临床评估潜力。

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