...
【24h】

Inhibition of mitochondrial respiratory chain in brain of rats subjected to an experimental model of depression.

机译:抑郁实验模型对大鼠脑线粒体呼吸链的抑制作用。

获取原文
获取原文并翻译 | 示例
           

摘要

Depressive disorders, including major depression, are serious and disabling. However, the exact pathophysiology of depression is not clearly understood. Life stressors contribute in some fashion to depression and are an extension of what occurs normally. In this context, chronic stress has been used as an animal model of depression. Based on the hypothesis that metabolism impairment might be involved in the pathophysiology of depression, in the present work we evaluated the activities of mitochondrial respiratory chain complexes and creatine kinase in brain of rats subjected to chronic stress. After 40 days of mild stress, a reduction in sweet food ingestion was observed, as well as increased adrenal gland weight, when compared to control group. We also verified that control group gained weight after 40 days, but stressed group did not. Moreover, our findings showed that complex I, III and IV were inhibited in stress group only in cerebral cortex and cerebellum. On the other hand, complex II and creatine kinase were not affected in stressed group. Although it is difficult to extrapolate our findings to the human condition, the inhibition of mitochondrial respiratory chain by chronic stress may be one mechanism in the pathophysiology of depressive disorders.
机译:包括重度抑郁症在内的抑郁症很严重且致残。但是,抑郁症的确切病理生理学还不清楚。生活压力源以某种方式加剧了抑郁症,是正常情况下的延伸。在这种情况下,慢性应激已被用作抑郁症的动物模型。基于代谢障碍可能与抑郁症的病理生理有关的假说,在本研究中,我们评估了慢性应激大鼠脑线粒体呼吸链复合物和肌酸激酶的活性。与对照组相比,轻度应激40天后,甜食摄入减少,肾上腺重量增加。我们还验证了对照组在40天后体重增加,而压力组却没有。而且,我们的研究结果表明,复合物I,III和IV仅在应激组中被抑制,仅在大脑皮层和小脑中。另一方面,复合物II和肌酸激酶在应激组中不受影响。尽管很难将我们的发现推论到人类的病情上,但是慢性应激对线粒体呼吸链的抑制可能是抑郁症的病理生理机制之一。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号