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The protective and therapeutic effects of vinpocetine, a PDE1 inhibitor, on oxidative stress and learning and memory impairment induced by an intracerebroventricular (ICV) injection of amyloid beta (aβ) peptide.
Behavioural Brain Research ( IF 2.7 ) Pub Date : 2020-01-25 , DOI: 10.1016/j.bbr.2020.112512
Meysam Shekarian 1 , Alireza Komaki 2 , Siamak Shahidi 1 , Abdolrahman Sarihi 1 , Iraj Salehi 1 , Safoura Raoufi 1
Affiliation  

Alzheimer's disease (AD) is a neurodegenerative disease leading to cognitive and memory impairment. This study aimed at investigating the therapeutic and preserving effects of vinpocetine on amyloid beta (Aβ)-induced rat model of AD. Sixty male adult Wistar rats were randomly divided into 6 groups (n = 10 per group) as follows: 1; control, 2; sham, 3; Aβ, 4; pre-treatment (vinpocetine + Aβ): oral gavage administration of vinpocetine at 4 mg/kg for 30 days followed by intracerebroventricular (ICV) injection of Aβ, 5; treatment (Aβ + vinpocetine): Aβ ICV injection followed by vinpocetine administration for 30 days, 6; pre-treatment + treatment (vinpocetine + Aβ + vinpocetine): vinpocetine administration for 30 days before and 30 days after AD induction. Following treatments, the animals' learning and memory were investigated using passive avoidance learning (PAL) task, Morris water maze (MWM), and novel object recognition (NOR) tests. The results demonstrated that Aβ significantly enhanced escape latency and the distance traveled in the MWM, decreased step-through latency, and increased time spent in the dark compartment in PAL. Vinpocetine ameliorated the Aβ-infused memory deficits in both MWM and PAL tests. Administration of vinpocetine in the Aβ rats increased the discrimination index of the NOR test. It also significantly diminished the nitric oxide and malondialdehyde levels and restored the reduced glutathione (GSH) levels. Vinpocetine can improve memory and learning impairment following Aβ infusion due to its different properties, including antioxidant effects, which indicates that vinpocetine administration can lead to the amelioration of cognitive dysfunction in AD.

中文翻译:

PDE1抑制剂长春西汀对脑室内(ICV)注射淀粉样β(aβ)肽引起的氧化应激和学习记忆障碍的保护和治疗作用。

阿尔茨海默氏病(AD)是导致认知和记忆障碍的神经退行性疾病。这项研究旨在调查长春西汀对淀粉样蛋白β(Aβ)诱导的AD大鼠模型的治疗和保存作用。将六十只成年雄性Wistar大鼠随机分为6组(每组n = 10),如下:1;控制2; 假3 Aβ,4;预处理(长春西汀+Aβ):以4 mg / kg的长春西汀口服管饲30天,然后脑室内(ICV)注射Aβ,5;治疗(Aβ+长春西汀):AβICV注射,然后长春西汀给药30天,6;预处理+治疗(长春西汀+Aβ+长春西汀):长春西汀在诱导AD前30天和之后30天给药。经过治疗,动物的 使用被动回避学习(PAL)任务,莫里斯水迷宫(MWM)和新型对象识别(NOR)测试对学习和记忆进行了研究。结果表明,Aβ显着增加了逃逸潜伏期和在MWM中行进的距离,降低了穿越潜伏期,并增加了在PAL中黑暗隔间中度过的时间。长春西汀可改善MWM和PAL测试中Aβ注入的记忆缺陷。在Aβ大鼠中施用长春西汀可提高NOR试验的判别指数。它还显着降低了一氧化氮和丙二醛的水平,并恢复了降低的谷胱甘肽(GSH)水平。长春西汀由于其不同的特性(包括抗氧化剂作用)可以改善Aβ注入后的记忆力和学习障碍
更新日期:2020-01-26
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