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慢性变应原应激损害大鼠前额叶皮层和海马的能量代谢:慢性抗氧化治疗的预防作用。

Chronic variable stress impairs energy metabolism in prefrontal cortex and hippocampus of rats: prevention by chronic antioxidant treatment.

机构信息

Laboratório de Neuroproteção e Doenças Metabólicas, Porto Alegre, RS, CEP 90035-003, Brasil.

出版信息

Metab Brain Dis. 2010 Jun;25(2):169-76. doi: 10.1007/s11011-010-9194-x. Epub 2010 May 27.

DOI:10.1007/s11011-010-9194-x
PMID:20505986
Abstract

Since chronic stress has been used widely for studying clinical depression and that brain energy metabolism and oxidative stress might be involved in the pathophysiology of this illness, the objective of this study was investigate the activities of pyruvate kinase, complex II and IV (cytocrome c oxidase) in hippocampus and prefrontal cortex of rats submitted to chronic variable stress. We also evaluated if vitamins E and C administration could prevent such effects. During 40 days adult rats from the stressed group were subjected to one stressor per day, at a different time each day, in order to minimize predictability. The stressed group had gained less weight while its immobilization time in the forced swimming test was greater than that of the control group. Results showed that stressed group presented an inhibition in the activities of complex II and cytochrome c oxidase in prefrontal cortex, while in hippocampus just complex IV was inhibited. Pyruvate kinase activity was not altered in stressed group when compared to control. Vitamins E and C administration prevented the alterations on respiratory chain caused by stress. These data suggest that the impairment of energy metabolism and oxidative stress could be related with the pathogenic pathways in stress related disorders.

摘要

由于慢性应激广泛用于研究临床抑郁症,并且大脑能量代谢和氧化应激可能涉及该疾病的病理生理学,因此本研究的目的是研究慢性可变应激后大鼠海马体和前额叶皮层中丙酮酸激酶、复合物 II 和 IV(细胞色素 c 氧化酶)的活性。我们还评估了维生素 E 和 C 的给药是否可以预防这种作用。在 40 天的时间里,应激组的成年大鼠每天接受一种应激源,每天在不同的时间进行,以尽量减少可预测性。应激组的体重增加较少,而其在强迫游泳试验中的固定时间长于对照组。结果表明,应激组前额叶皮层中的复合物 II 和细胞色素 c 氧化酶活性受到抑制,而海马体中仅复合物 IV 受到抑制。与对照组相比,应激组的丙酮酸激酶活性没有改变。维生素 E 和 C 的给药可防止应激引起的呼吸链改变。这些数据表明,能量代谢和氧化应激的损害可能与应激相关疾病的发病途径有关。

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