Tianeptine exerts neuroprotective effects in the brain tissue of rats exposed to the chronic stress model

Della, Franciela P.; Abelaira, Helena M.; Réus, Gislaine Z.; Antunes, Altamir Rocha; Santos, Maria Augusta B Dos; Zappelinni, Giovanni; Steckert, Amanda V.; Vuolo, Francieli; Galant, Letícia Selinger; Dal‐Pizzol, Felipe; Kapczinski, Flávio; Quevedo, Joao L De

doi:10.1016/j.pbb.2012.09.018

Cited by 34 publications

(16 citation statements)

References 60 publications

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“…In a single stress rat model, increased neuronal apoptosis has been observed in the medial prefrontal cortex (mPFC) 7 days after stress exposure indicating that apoptotic-related molecules are sensitive to traumatic stress (27). Emerging data indicate that TNF and the anti-apoptotic protein Bcl-2 exert a neuroprotective effect in the brain against traumatic stress (28–30). …”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Gene Expression Profiles and Metabolic Pathways in the Amygdala Associated with Exaggerated Fear in an Animal Model of PTSD

Smerin

et al. 2014

Front. Neurol.

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The metabolic mechanisms underlying the development of exaggerated fear in post-traumatic stress disorder (PTSD) are not well defined. In the present study, alteration in the expression of genes associated with mitochondrial function in the amygdala of an animal model of PTSD was determined. Amygdala tissue samples were excised from 10 non-stressed control rats and 10 stressed rats, 14 days post-stress treatment. Total RNA was isolated, cDNA was synthesized, and gene expression levels were determined using a cDNA microarray. During the development of the exaggerated fear associated with PTSD, 48 genes were found to be significantly upregulated and 37 were significantly downregulated in the amygdala complex based on stringent criteria (p < 0.01). Ingenuity pathway analysis revealed up- or downregulation in the amygdala complex of four signaling networks – one associated with inflammatory and apoptotic pathways, one with immune mediators and metabolism, one with transcriptional factors, and one with chromatin remodeling. Thus, informatics of a neuronal gene array allowed us to determine the expression profile of mitochondrial genes in the amygdala complex of an animal model of PTSD. The result is a further understanding of the metabolic and neuronal signaling mechanisms associated with delayed and exaggerated fear.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial Gene Expression Profiles and Metabolic Pathways in the Amygdala Associated with Exaggerated Fear in an Animal Model of PTSD

Smerin

et al. 2014

Front. Neurol.

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“…A decrease in raised lipid and protein peroxidation was seen after treatment with imipramine [63,64], desipramine [64], citalopram [64], escitalopram [45], fluoxetine [51,63], venlafaxine [46,63] and tianeptine [62]. Chronic treatment with imipramine also evoked a rise of TAC [61] and lipid hydroperoxide [60].…”

Section: Modulation Of Oxidative Balance By Antidepressant Drugsmentioning

confidence: 93%

“…A reduction of the TAC was seen in the cerebellum and nucleus accumbens in the bulbectomized rats, while an increase of this parameter was observed in the prefrontal cortex [61]. Lowered SOD activity was seen in several animal models [40,41,44,[47][48][49]51,52,[54][55][56][57]61,62], and its down-regulation seemed to be a general mechanism caused by exposure to chronic stress (see also [58,60]). The CAT activity either decreased following sleep deprivation [41,48,49,[51][52][53]62] or increased [40,58] (Table 1).…”

Section: Animal Studiesmentioning

confidence: 99%

“…A recovery of depleted GSH levels was seen after treatment with imipramine [63,64], desipramine [53,64], citalopram [53,64], escitalopram [45], fluoxetine [51,63] and venlafaxine [46,63]. Antidepressants with different mechanisms of actions evoked a recovery in the activities of SOD [51,[61][62][63], CAT [51,53,[62][63][64], GSH-Px [45,46], GSH-S-transferase and GSH-R [51,63] (Table 2). So, antidepressant drugs normalize the oxidant/antioxidant balance in the brain.…”

Section: Modulation Of Oxidative Balance By Antidepressant Drugsmentioning

confidence: 99%

“…-# SOD (prefrontal cortex, hippocampus, amygdala, nucleus accumbens) # CAT (nucleus accumbens) [62] " lipid peroxidation (cortex) " protein peroxidation (prefrontal cortex, amygdala)…”

Section: Diseasementioning

confidence: 99%

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Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism

Smaga

Niedzielska

Gawlik

et al. 2015

Pharmacological Reports

217

123

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The pathophysiology of psychiatric diseases, including depression, anxiety, schizophrenia and autism, is far from being fully elucidated. In recent years, a potential role of the oxidative stress has been highlighted in the pathogenesis of neuropsychiatric disorders. A body of clinical and preclinical evidence indicates that psychiatric diseases are characterized by higher levels of oxidative biomarkers and with lower levels of antioxidant defense biomarkers in the brain and peripheral tissues. In this article, we review current knowledge on the role of the oxidative stress in psychiatric diseases, based on clinical trials and animal studies, in addition, we analyze the effects of drug-induced modulation of oxidative balance and explore pharmacotherapeutic strategies for oxidative stress reduction.

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Antioxidant treatment ameliorates experimental diabetes‐induced depressive‐like behaviour and reduces oxidative stress in brain and pancreas

Réus

Santos

Abelaira

et al. 2015

Diabetes Metabolism Res

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Studies have shown a relationship between diabetes mellitus (DM) and the development of major depressive disorder. Alterations in oxidative stress are associated with the pathophysiology of both diabetes mellitus and major depressive disorder. This study aimed to evaluate the effects of antioxidants N-acetylcysteine and deferoxamine on behaviour and oxidative stress parameters in diabetic rats. To this aim, after induction of diabetes by a single dose of alloxan, Wistar rats were treated with N-acetylcysteine or deferoxamine for 14 days, and then depressive-like behaviour was evaluated. Oxidative stress parameters were assessed in the prefrontal cortex, hippocampus, amygdala, nucleus accumbens and pancreas. Diabetic rats displayed depressive-like behaviour, and treatment with N-acetylcysteine reversed this alteration. Carbonyl protein levels were increased in the prefrontal cortex, hippocampus and pancreas of diabetic rats, and both N-acetylcysteine and deferoxamine reversed these alterations. Lipid damage was increased in the prefrontal cortex, hippocampus, amygdala and pancreas; however, treatment with N-acetylcysteine or deferoxamine reversed lipid damage only in the hippocampus and pancreas. Superoxide dismutase activity was decreased in the amygdala, nucleus accumbens and pancreas of diabetic rats. In diabetic rats, there was a decrease in catalase enzyme activity in the prefrontal cortex, amygdala, nucleus accumbens and pancreas, but an increase in the hippocampus. Treatment with antioxidants did not have an effect on the activity of antioxidant enzymes. In conclusion, animal model of diabetes produced depressive-like behaviour and oxidative stress in the brain and periphery. Treatment with antioxidants could be a viable alternative to treat behavioural and biochemical alterations induced by diabetes.

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Tianeptine exerts neuroprotective effects in the brain tissue of rats exposed to the chronic stress model

Cited by 34 publications

References 60 publications

Mitochondrial Gene Expression Profiles and Metabolic Pathways in the Amygdala Associated with Exaggerated Fear in an Animal Model of PTSD

Mitochondrial Gene Expression Profiles and Metabolic Pathways in the Amygdala Associated with Exaggerated Fear in an Animal Model of PTSD

Oxidative stress as an etiological factor and a potential treatment target of psychiatric disorders. Part 2. Depression, anxiety, schizophrenia and autism

Antioxidant treatment ameliorates experimental diabetes‐induced depressive‐like behaviour and reduces oxidative stress in brain and pancreas

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