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胸腺醌对大鼠脂多糖诱导的海马细胞因子水平、脑氧化应激状态及记忆缺陷的影响。

The effects of thymoquinone on hippocampal cytokine level, brain oxidative stress status and memory deficits induced by lipopolysaccharide in rats.

作者信息

Bargi Rahimeh, Asgharzadeh Fereshteh, Beheshti Farimah, Hosseini Mahmoud, Sadeghnia Hamid Reza, Khazaei Majid

机构信息

Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

出版信息

Cytokine. 2017 Aug;96:173-184. doi: 10.1016/j.cyto.2017.04.015. Epub 2017 Apr 19.

Abstract

OBJECTIVE

The study objective was to determine the protective effects of thymoquinone (TQ) on brain tissues oxidative stress status, hippocampal cytokine level, and learning and memory deficits induced by lipopolysaccharide (LPS) in rats.

METHODS

Animals were randomly divided into the following groups and treated: (1) Control (saline), (2) LPS (1mg/kg i.p.), (3-5) 2, 5 or 10mg/kg TQ extract 30min before LPS injection. The treatment was started since two weeks before the behavioral experiments and continued during the behavioral tests (LPS injected 2h before each behavioral experiment). Finally, the brains were removed for biochemical assessments.

RESULTS

Morris water maze (MWM) test results showed that LPS increased escape latency compared to control group whereas TQ decreased them vs. LPS group. In passive avoidance (PA) test, LPS reduced the latency to enter the dark compartment vs. control group, while TQ treatment attenuated this effect of LPS. Additionally, LPS increased interleukin-6 (IL-6) and tumor necrosis alpha (TNF-α) in the hippocampal tissues. It also elevated malondialdehyde (MDA) and nitric oxide (NO) metabolites and decreased thiol content, superoxide dismutase (SOD) and catalase (CAT) in both hippocampus and cortex vs. control group, while TQ decreased IL-6, TNF-α, MDA and NO metabolites and increased thiol content, SOD and CAT compared to LPS group.

CONCLUSION

Findings of current study indicated that TQ improved LPS-induced learning and memory impairments induced by LPS in rats by attenuating the hippocampal cytokine levels and brain tissues oxidative damage.

摘要

目的

本研究旨在确定百里醌(TQ)对大鼠脑组织氧化应激状态、海马细胞因子水平以及脂多糖(LPS)诱导的学习和记忆缺陷的保护作用。

方法

将动物随机分为以下几组并进行处理:(1)对照组(生理盐水),(2)LPS组(腹腔注射1mg/kg),(3 - 5)在注射LPS前30分钟给予2、5或10mg/kg TQ提取物组。从行为实验前两周开始进行处理,并在行为测试期间持续(每次行为实验前2小时注射LPS)。最后,取出大脑进行生化评估。

结果

莫里斯水迷宫(MWM)测试结果显示,与对照组相比,LPS增加了逃避潜伏期,而与LPS组相比,TQ降低了逃避潜伏期。在被动回避(PA)测试中,与对照组相比,LPS缩短了进入暗室的潜伏期,而TQ处理减弱了LPS的这种作用。此外,LPS增加了海马组织中的白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)。与对照组相比,LPS还增加了海马和皮质中的丙二醛(MDA)和一氧化氮(NO)代谢产物,并降低了硫醇含量、超氧化物歧化酶(SOD)和过氧化氢酶(CAT),而与LPS组相比,TQ降低了IL-6、TNF-α、MDA和NO代谢产物,并增加了硫醇含量、SOD和CAT。

结论

本研究结果表明,TQ通过减弱海马细胞因子水平和脑组织氧化损伤,改善了LPS诱导的大鼠学习和记忆障碍。

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