氧化应激和炎症对焦虑和高血压的潜在贡献。
Potential contribution of oxidative stress and inflammation to anxiety and hypertension.
机构信息
Department of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, USA.
出版信息
Brain Res. 2011 Aug 2;1404:63-71. doi: 10.1016/j.brainres.2011.06.024. Epub 2011 Jun 16.
Abstract
Previously, we have published that pharmacological induction of oxidative stress causes anxiety-like behavior in rats and also is associated with hypertension in these animals. Here, we report that sub-chronic induction of oxidative stress via pharmacological induction leads to i) reduction in glyoxalase (GLO)-1 and glutathione reductase (GSR)-1 expression; ii) calpain mediated reduction of brain derived neurotrophic factor (BDNF) levels; iii) NFκB mediated upregulation of proinflammatory factors interleukin (IL)-6 and tumor necrosis factor (TNF)-α and elevated angiotensin (AT)-1 receptor levels in hippocampus, amygdala and locus coeruleus regions of the brain. Acute oxidative stress has opposite effects. We speculate that regulation of GLO1, GSR1, BDNF, NFκB and AT-1 receptor may contribute to anxiety-like behavior and hypertension in rats.
摘要
此前，我们发表了药理学诱导氧化应激会导致大鼠出现类似焦虑的行为，并且还与这些动物的高血压有关。在这里，我们报告称，通过药理学诱导进行亚慢性氧化应激诱导会导致：i） 糖氧化解酶 (GLO)-1 和谷胱甘肽还原酶 (GSR)-1 表达减少；ii） 钙蛋白酶介导的脑源性神经营养因子 (BDNF) 水平降低；iii） NFκB 介导的促炎因子白细胞介素 (IL)-6 和肿瘤坏死因子 (TNF)-α 上调以及血管紧张素 (AT)-1 受体水平升高，这些变化发生在海马体、杏仁核和蓝斑核区域的大脑中。急性氧化应激则具有相反的效果。我们推测，GLO1、GSR1、BDNF、NFκB 和 AT-1 受体的调节可能导致大鼠出现类似焦虑的行为和高血压。
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