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维生素 D3 给药可预防不可预知的慢性轻度应激诱导的大鼠记忆缺陷和生化参数改变。

Vitamin D3 administration prevents memory deficit and alteration of biochemical parameters induced by unpredictable chronic mild stress in rats.

机构信息

Student Research Committee, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran.

Neuroscience Research Center, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran.

出版信息

Sci Rep. 2021 Aug 11;11(1):16271. doi: 10.1038/s41598-021-95850-6.

DOI:10.1038/s41598-021-95850-6
PMID:34381124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8357828/
Abstract

The present study aimed to investigate the effects of vitamin D3 (Vit D) administration on memory function, hippocampal level of amyloid-beta (Aβ), brain-derived neurotrophic factor (BDNF) and oxidative stress status in a rat model of unpredictable chronic mild stress (UCMS). Vit D was intraperitoneally administered at doses of 100, 1000, and 10,000 IU/kg. Animals were subjected to UCMS for a total period of 4 weeks. Memory function was assessed using morris water maze (MWM) and passive avoidance (PA) tests. Biochemical markers were measured to reveal the status of oxidative stress and antioxidant defense system. In addition, the levels of Aβ and BDNF were measured in hippocampal region. In the UCMS group, latency to find the platform was greater and the time spent in target quadrant (MWM test) as well as the latency to enter the dark compartment (PA test), were less than the vehicle group. Hippocampal malondialdehyde (MDA) and Aβ concentrations in the UCMS group were higher than the vehicle group. Hippocampal level of thiol and BDNF plus the activities of catalase and superoxide dismutase (SOD) were reduced in UCMS group compared to the control subjects (i.e. vehicle group). Interestingly, Vit D treatment supplementation reversed the mentioned effects of UCMS. Our findings indicated that Vit D administration improves UCMS-induced impairment of learning and memory through prevention of adverse effects on Aβ, BDNF and oxidative stress parameters.

摘要

本研究旨在探讨维生素 D3(Vit D)给药对不可预测慢性轻度应激(UCMS)大鼠模型中记忆功能、海马淀粉样蛋白-β(Aβ)、脑源性神经营养因子(BDNF)和氧化应激状态的影响。Vit D 通过腹腔内给药,剂量分别为 100、1000 和 10000 IU/kg。动物接受 UCMS 处理总周期为 4 周。使用 Morris 水迷宫(MWM)和被动回避(PA)测试评估记忆功能。测量生化标志物以揭示氧化应激和抗氧化防御系统的状态。此外,还测量了海马区的 Aβ和 BDNF 水平。在 UCMS 组中,找到平台的潜伏期较长,目标象限停留时间(MWM 测试)以及进入暗室的潜伏期(PA 测试)比载体组短。与载体组相比,UCMS 组海马丙二醛(MDA)和 Aβ浓度较高。与对照组(即载体组)相比,UCMS 组的海马硫醇水平和 BDNF 加上过氧化氢酶和超氧化物歧化酶(SOD)的活性降低。有趣的是,Vit D 治疗补充逆转了 UCMS 的上述作用。我们的研究结果表明,Vit D 给药通过预防 Aβ、BDNF 和氧化应激参数的不良反应,改善了 UCMS 诱导的学习和记忆损伤。

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