Minocycline protects against oxidative damage and alters energy metabolism parameters in the brain of rats subjected to chronic mild stress

Abstract

Studies have been suggested that minocycline can be a potential new agent for the treatment of depression. In addition, both oxidative stress and energy metabolism present an important role in pathophysiology of depression. So, the present study was aimed to evaluate the effects of minocycline on stress oxidative parameters and energy metabolism in the brain of adult rats submitted to the chronic mild stress protocol (CMS). After CMS Wistar, both stressed animals as controls received twice ICV injection of minocycline (160 μg) or vehicle. The oxidative stress and energy metabolism parameters were assessed in the prefrontal cortex (PF), hippocampus (HIP), amygdala (AMY) and nucleus accumbens (Nac). Our findings showed that stress induced an increase on protein carbonyl in the PF, AMY and NAc, and mynocicline injection reversed this alteration. The TBARS was increased by stress in the PF, HIP and NAc, however, minocycline reversed the alteration in the PF and HIP. The Complex I was incrased in AMY by stress, and minocycline reversed this effect, however reduced Complex I activity in the NAc; Complex II reduced in PF and AMY by stress or minocycline; the Complex II-III increased in the HIP in stress plus minocycline treatment and in the NAc with minocycline; in the PF and HIP there were a reduced in Complex IV with stress and minocycline. The creatine kinase was reduced in AMY and NAc with stress and minocycline. In conclusion, minocycline presented neuroprotector effects by reducing oxidative damage and regulating energy metabolism in specific brain areas.

LC/QTOF profile and preliminary stability studies of an enriched flavonoid fraction of Cecropia pachystachya Trécul leaves with potential antidepressant‐like activity

“…However, these alterations are dependent on treatment, mitochondrial complex and brain area studied. Previous studies showed that the chronic mild stress protocol altered energy metabolism in the rat brain and chronic treatment with minocycline regulated these alterations in specific brain areas (Réus, Abelaira, et al, ). Abelaira et al () showed that acute and chronic treatment with lamotrigine prevented mitochondrial dysfunction by increasing complex II, II–III and IV activities in rat brain.…”

“…Emerging evidence suggests a significant role for mitochondrial dysfunction, oxidative stress and inflammation as the main contributors to the neuronal damage that is observed in major depressive disorder (MDD) (Bakunina, Pariante, & Zunszain, ; Morris & Berk, ). On the other hand, antidepressants might decrease inflammatory and oxidative damage and improve mitochondrial dysfunction in animal models of depression (Réus, Abelaira, et al, ; Réus, Carlessi, et al, ) and in depressed patients (Behr, Moreira, & Frey, ; Lee et al, ). Furthermore, current antidepressants have major shortcomings that include slow onset of action, poor efficacy and unwanted side effects, the search for new and improved antidepressants is still relevant (El‐Alfy, Abourashed, & Matsumoto, ).…”

Neuroinflammatory reactions in sickness behavior induced by bacterial infection: Protective effect of minocycline

“…MIN also protects dopaminergic neurons from the activation of microglia induced by an injection of LPS within the substantia nigra . MIN may not directly impact the serotonergic system; and may produce its effect through modification of the noradrenergic system in the brain …”

Effects of previous physical exercise to chronic stress on long‐term aversive memory and oxidative stress in amygdala and hippocampus of rats

“…Since physical exercise may improve oxidative status and memory (Lee et al, 2013; Liu and Zhou, 2012; Patki et al, 2014; Yau et al, 2015) and studies show that CVS induces oxidative stress and impairs Na + , K + ‐ATPase and memory (De Vasconcellos et al, 2005; Della et al, 2012; Gamaro et al, 2003; Patki et al, 2014; Réus et al, 2015; Tagliari et al, 2011a, 2011b, 2010b), and that antioxidants prevent energy metabolism and memory deficits caused by CVS (Tagliari et al, 2011b, 2010b), in the present study we decided to test the protective effect of physical exercise on behavioral and biochemical changes caused by CVS.…”