COVID-19, Oxidative Stress, and Neuroinflammation in the Depression Route

被引:36
作者
Dama Mingoti, Maiqueli Eduarda [1 ]
Bertollo, Amanda Gollo [1 ]
Batista Simoes, Julia Leao [2 ]
Francisco, Gabriel Rossi [2 ]
Bagatini, Margarete Dulce [2 ]
Ignacio, Zuleide Maria [1 ]
机构
[1] Fed Univ Fronteira Sul, Lab Physiol Pharmacol & Psychopathol, Grad Program Biomed Sci, BR-89815899 Chapeco, SC, Brazil
[2] Fed Univ Fronteira Sul, Lab Cell Culture, Grad Program Biomed Sci, BR-89815899 Chapeco, SC, Brazil
关键词
COVID-19; Oxidative stress; Neuroinflammation; Glial activation; Major depressive disorder; QUINOLINIC ACID; CYTOKINE STORM; INFLAMMATION; CORONAVIRUS; RECEPTOR; INFECTION; DISORDER; SYSTEM; ACE2; TRYPTOPHAN;
D O I
10.1007/s12031-022-02004-y
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
COVID-19 is associated with oxidative stress, peripheral hyper inflammation, and neuroinflammation, especially in individuals with a more severe form of the disease. Some studies provide evidence on the onset or exacerbation of major depressive disorder (MDD), among other psychiatric disorders due to COVID-19. Oxidative stress and neuroinflammation are associated conditions, especially in the more severe form of MDD and in refractoriness to available therapeutic strategies. Inflammatory cytokines in the COVID-19 hyper inflammation process can activate the hypothalamic-pituitary-adrenal (HPA) axis and the indoleamine-2,3-dioxygenase (IDO) enzyme. IDO activation can reduce tryptophan and increase toxic metabolites of the kynurenine pathway, which increases glial activation, neuroinflammation, toxicity, and neuronal death. This review surveyed a number of studies and analyzed the mechanisms of oxidative stress, inflammation, and neuroinflammation involved in COVID-19 and depression. Finally, the importance of more protocols that can help elucidate the interaction between these mechanisms underlying COVID-19 and MDD and the possible therapeutic strategies involved in the interaction of these mechanisms are highlighted.
引用
收藏
页码:1166 / 1181
页数:16
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