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Depression anxiety-like behavior and memory impairment are associated with increased oxidative stress and inflammation in a rat model of social stress

机译:在社交压力的大鼠模型中抑郁焦虑样行为和记忆障碍与氧化应激和炎症增加相关

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摘要

In the present study, we have examined the behavioral and biochemical effect of induction of psychological stress using a modified version of the resident-intruder model for social stress (social defeat). At the end of the social defeat protocol, body weights, food and water intake were recorded, depression and anxiety-like behaviors as well as learning-memory function was examined. Biochemical analysis including oxidative stress measurement, inflammatory markers and other molecular parameters, critical to behavioral effects were examined. We observed a significant decrease in the body weight in the socially defeated rats as compared to the controls. Furthermore, social defeat increased anxiety-like behavior and caused memory impairment in rats (P<0.05). Socially defeated rats made significantly more errors in long term memory tests (P<0.05) as compared to control rats. Furthermore, brain extracellular signal-regulated kinase-1/2 (ERK1/2), and an inflammatory marker, interleukin (IL)-6 were activated (P<0.05), while the protein levels of glyoxalase (GLO)-1, glutathione reductase (GSR)-1, calcium/calmodulin-dependent protein kinase type (CAMK)-IV, cAMP-response-element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) were significantly less (P<0.05) in the hippocampus, but not in the prefrontal cortex and amygdala of socially defeated rats, when compared to control rats. We suggest that social defeat stress alters ERK1/2, IL-6, GLO1, GSR1, CAMKIV, CREB, and BDNF levels in specific brain areas, leading to oxidative stress-induced anxiety-depression-like behaviors and as well as memory impairment in rats.
机译:在本研究中,我们使用针对社会压力(社会失败)的居民-入侵者模型的修改版,研究了诱导心理压力的行为和生化作用。在社交失败协议结束时,记录体重,食物和水的摄入量,检查抑郁和焦虑样行为以及学习记忆功能。生化分析包括氧化应激测量,炎症标记和其他分子参数,对行为影响至关重要。我们观察到与对照组相比,在社会上失败的大鼠中体重显着降低。此外,社交失败增加了大鼠的焦虑样行为,并引起了记忆障碍(P <0.05)。与对照组相比,在社交记忆力下降的大鼠中,长期记忆测试的错误率更高(P <0.05)。此外,大脑细胞外信号调节激酶-1/2(ERK1 / 2)和炎症标记物白介素(IL)-6被激活(P <0.05),而乙二醛酶(GLO)-1,谷胱甘肽的蛋白水平还原酶(GSR)-1,钙/钙调蛋白依赖性蛋白激酶类型(CAMK)-IV,cAMP反应元件结合蛋白(CREB)和脑源性神经营养因子(BDNF)均显着减少(P <0.05)与对照大鼠相比,社交失败的大鼠的海马体,但不在前额叶皮层和杏仁核中。我们建议社交失败压力会改变特定脑区的ERK1 / 2,IL-6,GLO1,GSR1,CAMKIV,CREB和BDNF水平,从而导致氧化应激诱导的焦虑抑郁样行为以及记忆障碍大鼠。

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