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Oxidative stress in psychiatric disorders: evidence base and therapeutic implications.精神疾病中的氧化应激:证据基础与治疗意义。
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Stress increases vulnerability to inflammation in the rat prefrontal cortex.压力会增加大鼠前额叶皮质对炎症的易感性。
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Effects of chronic treatment with escitalopram or citalopram on extracellular 5-HT in the prefrontal cortex of rats: role of 5-HT1A receptors.艾司西酞普兰或西酞普兰长期治疗对大鼠前额叶皮质细胞外5-羟色胺的影响:5-羟色胺1A受体的作用
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Biological mechanisms in the relationship between depression and heart disease.抑郁症与心脏病关系中的生物学机制。
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Regulation of adult neurogenesis by antidepressant treatment.抗抑郁治疗对成体神经发生的调节作用。
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Measures of prefrontal system dysfunction in posttraumatic stress disorder.
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Antidepressants upregulate messenger RNA levels of the neuroprotective enzyme superoxide dismutase (SOD1).抗抑郁药可上调神经保护酶超氧化物歧化酶(SOD1)的信使核糖核酸水平。
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Oxidative stress and haematological changes in immobilized rats.固定不动大鼠的氧化应激与血液学变化
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Circadian rhythms and depression: effects of exercise in an animal model.昼夜节律与抑郁症:运动在动物模型中的作用
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Modification of ion homeostasis by lipid peroxidation: roles in neuronal degeneration and adaptive plasticity.脂质过氧化对离子稳态的修饰:在神经元变性和适应性可塑性中的作用。
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艾司西酞普兰对慢性轻度应激白化大鼠前额叶皮质和伏隔核中γ-氨基丁酸水平及抗氧化标志物的影响。

Effect of Escitalopram on GABA level and anti-oxidant markers in prefrontal cortex and nucleus accumbens of chronic mild stress-exposed albino rats.

作者信息

Shalaby Amany, Kamal Sahar

出版信息

Int J Physiol Pathophysiol Pharmacol. 2009 Jun 20;1(2):154-161.

PMID:21383885
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3047246/
Abstract

Oxidative stress is a critical route of damage in various psychological stress-induced disorders, such as depression. Antidepressants are widely prescribed to treat these conditions; however, few animal studies have investigated the effect of these drugs on endogenous antioxidant status in the brain. The present study employed a 3 weeks chronic regimen of random exposure to chronic mild stress (CMS) to induce oxidative stress in brain, and behavioural aberrations (anhedonia), in rats. The sucrose preference test was used to identify depression-like phenotypes, and reversal in these indices indicated the effectiveness of treatment with escitalopram 2.5mg/kg daily orally following CMS. The level of superoxide dismutase enzyme(SOD) as an antioxidant markers in erythrocyte lysates was reduced in CMS control group while it was elevated in CMS group treated with escitalopram. Also escitalopram significantly reduce the thiobarbituric acid reactive substance(TBARS) levels in selected brain areas homogenates to a level comparable to control group. Catalase activity and GABA levels in these brain areas were also increase in escitlopram treated group. In conclusion, escitalopram is suggested to have antioxidant effect associated with an increase in GABA level in frontal cortices and nucleus accumbens homogenates from rats exposed to CMS.

摘要

氧化应激是各种心理应激诱导的疾病(如抑郁症)中损伤的关键途径。抗抑郁药被广泛用于治疗这些疾病;然而,很少有动物研究调查这些药物对大脑内源性抗氧化状态的影响。本研究采用3周的慢性随机暴露于慢性轻度应激(CMS)方案,以诱导大鼠大脑中的氧化应激和行为异常(快感缺失)。蔗糖偏好试验用于识别类似抑郁的表型,这些指标的逆转表明每天口服2.5mg/kg艾司西酞普兰治疗CMS后有效。在CMS对照组中,作为红细胞裂解物中抗氧化标志物的超氧化物歧化酶(SOD)水平降低,而在用艾司西酞普兰治疗的CMS组中升高。此外,艾司西酞普兰显著降低所选脑区匀浆中的硫代巴比妥酸反应物质(TBARS)水平,使其与对照组相当。在这些脑区中,过氧化氢酶活性和GABA水平在用艾司西酞普兰治疗的组中也增加。总之,提示艾司西酞普兰具有抗氧化作用,这与暴露于CMS的大鼠额叶皮质和伏隔核匀浆中GABA水平的增加有关。