Aspirin inhibits stress-induced increase in plasma glutamate, brain oxidative damage and ATP fall in rats

被引:32
作者
De Cristóbal, J [1 ]
Madrigal, JLM [1 ]
Lizasoain, I [1 ]
Lorenzo, P [1 ]
Leza, JC [1 ]
Moro, MA [1 ]
机构
[1] Univ Complutense, Fac Med, Dept Farmacol, E-28040 Madrid, Spain
关键词
ATP; glutathione; immobilisation; iNOS; lipid peroxidation; NF-kappa B; restraint; stress-induced neurodegeneration; TNF-alpha;
D O I
10.1097/00001756-200202110-00009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The precise mechanisms by which stress induces brain damage are still being elucidated. The high-output, inducible isoform of nitric oxide (NO) synthase (NOS) is expressed in rat brain after immobilisation stress and its inhibition protects against cell damage in this condition. We have hereby explored some mechanisms involved in NOS expression and studied the effects of aspirin, a NSAID with neuroprotective actions, in this model. Acute (6 h) stress exposure in rats caused brain expression of NOS, an increase in plasma glutamate and brain TNF-alpha, induction of oxidative indicators in brain and a fall in brain ATP levels. Prior administration Of aspirin (10 mg/kg i.p.) inhibited all these effects caused by stress, suggesting possible therapeutic implications of this drug in this condition. NeuroReport 13:217-221 (C) 2002 Lippincott Williams Wilkins.
引用
收藏
页码:217 / 221
页数:5
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