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Chronic Stress Differentially Affects Antioxidant Enzymes and Modifies the Acute Stress Response in Liver of Wistar Rats

机译:慢性应激差异影响抗氧化酶并修饰Wistar大鼠肝脏的急性应激反应

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摘要

Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx.
机译:临床报告表明,应激源(尤其是持续时间较长的应激源)与肝脏疾病(例如肝炎)之间的紧密相互作用被认为是通过活性氧而发生的。在本研究中,我们将雄性Wistar大鼠的21天社会隔离作为慢性应激的模型,以研究肝脏抗氧化酶的蛋白表达/活性:超氧化物歧化酶(SOD),过氧化氢酶(CAT),谷胱甘肽过氧化物酶(GPx)和谷胱甘肽还原酶(GLR)及其上游调节子的蛋白表达:糖皮质激素受体(GR)和核因子κB(NFkB)。我们还对天真或慢性应激动物中受到30分钟急性固定挑战的这些参数进行了表征。我们发现慢性隔离导致血清皮质酮(CORT)和血糖(GLU)降低,NFkB信号增加以及CuZnSOD,过氧化物酶(CAT,GPx)和GLR之间的歧化,从而促进肝脏中H2O2的积累和过氧化状态。总体结果表明,慢性应激在CORT和GLU水平上夸大了对后续应激源的反应,并增强了GLR反应,但由于MnSOD和GPx的不可逆变化而损害了氧化还原平衡的恢复。

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