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Inflammopharmacology. 2015 Dec;23(6):291-305. doi: 10.1007/s10787-015-0238-z. Epub 2015 Jun 30.

本文引用的文献

1
Stress-induced neuroinflammation: mechanisms and new pharmacological targets.应激诱导的神经炎症:机制与新的药理学靶点。
Braz J Med Biol Res. 2008 Dec;41(12):1037-46. doi: 10.1590/s0100-879x2008001200001.
2
Inflammatory and oxidative and nitrosative stress pathways underpinning chronic fatigue, somatization and psychosomatic symptoms.支撑慢性疲劳、躯体化及身心症状的炎症、氧化和亚硝化应激途径。
Curr Opin Psychiatry. 2009 Jan;22(1):75-83. doi: 10.1097/yco.0b013e32831a4728.
3
Nitric oxide modulation mediates the protective effect of trazodone in a mouse model of chronic fatigue syndrome.一氧化氮调节介导了曲唑酮在慢性疲劳综合征小鼠模型中的保护作用。
Pharmacol Rep. 2008 Sep-Oct;60(5):664-72.
4
Immunological aspects of chronic fatigue syndrome.慢性疲劳综合征的免疫学方面
Autoimmun Rev. 2009 Feb;8(4):287-91. doi: 10.1016/j.autrev.2008.08.003. Epub 2008 Sep 16.
5
Neuroaetiology of chronic fatigue syndrome: an overview.慢性疲劳综合征的神经病因学:综述
World J Biol Psychiatry. 2008;9(3):165-71. doi: 10.1080/15622970701310971.
6
Not in the mind but in the cell: increased production of cyclo-oxygenase-2 and inducible NO synthase in chronic fatigue syndrome.不在大脑,而在细胞中:慢性疲劳综合征中环氧化酶-2和诱导型一氧化氮合酶的产生增加。
Neuro Endocrinol Lett. 2007 Aug;28(4):463-9.
7
Protective effect of alprazolam in acute immobilization stress-induced certain behavioral and biochemical alterations in mice.阿普唑仑对急性制动应激诱导的小鼠某些行为和生化改变的保护作用。
Pharmacol Rep. 2007 May-Jun;59(3):284-90.
8
Inhibitor of cyclooxygenase-2 protects against amyloid beta peptide-evoked memory impairment in mice.环氧化酶-2抑制剂可保护小鼠免受β-淀粉样肽诱发的记忆损伤。
Pharmacol Rep. 2007 Mar-Apr;59(2):164-72.
9
Cortisol levels and anxiety-related behaviors in cattle.牛的皮质醇水平与焦虑相关行为
Physiol Behav. 2007 Mar 16;90(4):626-8. doi: 10.1016/j.physbeh.2006.11.015. Epub 2006 Dec 29.
10
Erythrocyte oxidative damage in chronic fatigue syndrome.慢性疲劳综合征中的红细胞氧化损伤
Arch Med Res. 2007 Jan;38(1):94-8. doi: 10.1016/j.arcmed.2006.06.008. Epub 2006 Nov 3.

选择性和非选择性环氧化酶抑制剂在慢性应激动物模型中的保护作用。

Protective effects of selective and non-selective cyclooxygenase inhibitors in an animal model of chronic stress.

机构信息

University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh 160014, India.

出版信息

Neurosci Bull. 2010 Feb;26(1):17-27. doi: 10.1007/s12264-010-0713-x.

DOI:10.1007/s12264-010-0713-x
PMID:20101269
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5560377/
Abstract

OBJECTIVE

Cyclooxygenase isoenzyme is known to be expressed in different regions of brain, and is mainly used for the treatment of pain and inflammation. Recently, it is proposed that cyclooxygenase isoenzyme may also play a key role in the pathophysiology of various brain-related disorders. The present study was aimed to explore the protective effect of cyclooxygenase inhibitors on stress by using an animal model of chronic stress.

METHODS

The animals were forced to swim individually for a period of 6 min every day for 15 d. Then, the behavior (locomotor activity, anxiety and memory) and biochemical (lipid peroxidation, nitrite level, reduced glutathione, and catalase) alterations were assessed.

RESULTS

Forced swimming for 15 d caused impaired locomotor activity, anxiety-like behavior and decreased percentage of memory retention, as compared to naive mice (without chronic fatigue treatment). Biochemical analysis revealed significant increases in lipid peroxidation and nitrite level, while levels of reduced glutathione and catalase activity were both decreased. Chronic treatment with naproxen (14 mg/kg, i.p.), rofecoxib (5 mg/kg, i.p.), meloxicam (5 mg/kg, i.p.), nimesulide (5 mg/kg, i.p.) and valdecoxib (10 mg/kg, i.p.) significantly attenuated these behavioral and biochemical (oxidative damage) alterations in chronic-stressed mice.

CONCLUSION

The cyclooxygenase inhibitors could be used in the management of chronic fatigue-like conditions.

摘要

目的

环氧化酶同工酶已知在大脑的不同区域表达,主要用于治疗疼痛和炎症。最近,有人提出环氧化酶同工酶也可能在各种与大脑相关的疾病的病理生理学中发挥关键作用。本研究旨在通过使用慢性应激动物模型来探索环氧化酶抑制剂对应激的保护作用。

方法

动物每天被迫单独游泳 6 分钟,持续 15 天。然后评估行为(运动活动、焦虑和记忆)和生化(脂质过氧化、亚硝酸盐水平、还原型谷胱甘肽和过氧化氢酶)变化。

结果

与未接受慢性疲劳治疗的对照(无慢性疲劳处理)相比,15 天的强迫游泳导致运动活动受损、焦虑样行为和记忆保留百分比降低。生化分析显示脂质过氧化和亚硝酸盐水平显著升高,而还原型谷胱甘肽和过氧化氢酶活性水平均降低。萘普生(14mg/kg,腹腔注射)、罗非昔布(5mg/kg,腹腔注射)、美洛昔康(5mg/kg,腹腔注射)、尼美舒利(5mg/kg,腹腔注射)和伐地昔布(10mg/kg,腹腔注射)的慢性治疗显著减轻了慢性应激小鼠的这些行为和生化(氧化损伤)改变。

结论

环氧化酶抑制剂可用于管理慢性疲劳样疾病。